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3a womens health > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

What is Androgen insensitivity syndrome?

A

X-linked recessive condition due to end-organ resistance to testosterone

mutation in the androgen receptor gene

causing genotypically male children (46XY) to have a female phenotype

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2
Q

What are the features of Androgen insensitivity syndrome?

A

‘primary amenorrhoea’
little or no axillary and pubic hair
undescended testes causing groin swellings
breast development may occur as a result of the conversion of testosterone to oestradiol

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3
Q

How is Androgen insensitivity syndrome diagnosed?

A

buccal smear or chromosomal analysis to reveal 46XY genotype
after puberty, testosterone concentrations are in the high-normal to slightly elevated reference range for postpubertal boys

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4
Q

What would hormone results for Androgen insensitivity syndrome show

A

Raised LH
Normal or raised FSH
Normal or raised testosterone levels (for a male)
Raised oestrogen levels (for a male)

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5
Q

How is Androgen insensitivity syndrome managed?

A

counselling - raise the child as female
bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
oestrogen therapy

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6
Q

What is Adenomyosis

A

endometrial tissue within the myometrium

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7
Q

Who is Adenomyosis more common in

A

multiparous women towards the end of their reproductive years

It may occur alone, or alongside endometriosis or fibroids.

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8
Q

What conditions tend to resolve after menopause

A

Adenomyosis endometriosis and fibroids.

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9
Q

How does Adenomyosis present

A

Painful periods (dysmenorrhoea)
Heavy periods (menorrhagia)
Pain during intercourse (dyspareunia)

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10
Q

How would Adenomyosis feel on examination

A

an enlarged and tender uterus.

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11
Q

What is first line investigation for Adenomyosis

A

Transvaginal ultrasound

MRI and transabdominal ultrasound are alternative investigations

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12
Q

What is the gold standard investigation for Adenomyosis

A

histological examination of the uterus after a hysterectomy

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13
Q

How is Adenomyosis managed when the woman does not want contraception

A

Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)

Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

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14
Q

How is Adenomyosis managed when contraception is wanted

A

Mirena coil (first line)
Combined oral contraceptive pill
Cyclical oral progestogens

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15
Q

What are other management options of Adenomyosis beside tranexamic acid and contraception

A

GnRH analogues to induce a menopause-like state
Endometrial ablation
Uterine artery embolisation
Hysterectomy

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16
Q

What conditions are associated with Adenomyosis

A

Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for caesarean section
Postpartum haemorrhage

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17
Q

What is Atrophic Vaginitis

A

dryness and atrophy of the vaginal mucosa related to a lack of oestrogen

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18
Q

Who does Atrophic Vaginitis occur in

A

post menopausal

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19
Q

how does Atrophic Vaginitis present

A

Itching
Dryness
Dyspareunia (discomfort or pain during sex)
Bleeding due to localised inflammation

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20
Q

how does Atrophic Vaginitis appear on examination

A

Pale mucosa
Thin skin
Reduced skin folds
Erythema and inflammation
Dryness
Sparse pubic hair

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21
Q

how is Atrophic Vaginitis managed

A

Vaginal lubricants - Sylk, Replens and YES
Topical oestrogen - cream, pessaries, tablets, ring

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22
Q

What is Asherman’s Syndrome

A

adhesions (sometimes called synechiae) form within the uterus, following damage to the uterus and form physical obstructions and distort the pelvic organ

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23
Q

When does Asherman’s Syndrome occur

A

typically presents following recent dilatation and curettage, uterine surgery or endometritis

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24
Q

How does Asherman’s Syndrome present

A

Secondary amenorrhoea (absent periods)
Significantly lighter periods
Dysmenorrhoea (painful periods)

sometimes infertility

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25
Q

What is the gold standard investigation for Asherman’s Syndrome

A

Hysteroscopy

can involve dissection and treatment of the adhesions

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26
Q

Other than Hysteroscopy how else can Asherman’s Syndrome be investigated

A

Hysterosalpingography - contrast is injected into the uterus and imaged with xrays
Sonohysterography - uterus is filled with fluid & ultrasound
MRI

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27
Q

How is Asherman’s Syndrome managed

A

dissecting the adhesions during hysteroscopy

reoccurrence is common

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28
Q

why males do not develop a uterus

A

anti-Mullerian hormone

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29
Q

What structure in a fetus do congenital structural abnormality refer to

A

Mullerian ducts.

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30
Q

Name 4 congenital structural abnormality

A

Bicornuate Uterus
Imperforate Hymen
Transverse Vaginal Septae
Vaginal Hypoplasia and Agenesis

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31
Q

What is a Bicornuate Uterus

A

two “horns” to the uterus, giving the uterus a heart-shaped appearance.

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32
Q

What are typical complications of Bicornuate Uterus

A

Miscarriage
Premature birth
Malpresentation

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33
Q

What is a Imperforate Hymen

A

the hymen at the entrance of the vagina is fully formed, without an opening.

causes cyclical pelvic pain and cramping, but without any vaginal bleeding

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34
Q

How is Imperforate Hymen diagnosed and treatmed

A

diagnosed during a clinical examination. treated with surgical incision

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35
Q

What is a complication of untreated Imperforate Hymen

A

retrograde menstruation leading to endometriosis.

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36
Q

What is a Transverse Vaginal Septae

A

a wall forms transversely across the vagina. This septum can either be perforate or imperforate

perforate = still menstruate, but can have difficulty with intercourse or tampon use. imperforate = present similarly to an imperforate hymen

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37
Q

What are complications of transverse Vaginal Septae

A

infertility and pregnancy-related complications

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38
Q

How is transverse Vaginal Septae diagnosed

A

examination, ultrasound or MRI.

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39
Q

How is transverse Vaginal Septae treated and what is the complication of treatment

A

surgical correction

The main complications of surgery are vaginal stenosis and recurrence of the septae.

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40
Q

What is Vaginal hypoplasia

A

abnormally small vagina

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41
Q

What is Vaginal agenesis

A

an absent vagina.

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42
Q

What causes Vaginal Hypoplasia and Agenesis

A

failure of the Mullerian ducts to properly develop

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43
Q

Are ovaries affected in Vaginal Hypoplasia and Agenesis

A

ovaries are usually unaffected, leading to normal female sex hormones.

The exception to this is with androgen insensitivity syndrome, where there are testes rather than ovaries.

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44
Q

How is Vaginal Hypoplasia and Agenesis managed

A

use of a vaginal dilator over a prolonged period to create an adequate vaginal size. Alternatively, vaginal surgery may be necessary.

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45
Q

What is cervical cancer

A

80% are squamous cell carcinoma
adenocarcinoma next most common
strongly associated with human papillomavirus

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46
Q

When are children vax against HPV

A

12-13

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47
Q

What is used to screen for precancerous and cancerous changes to the cells of cervix

A

Cervical screening with smear tests

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48
Q

What is the most common cause of cervical cancer

A

human papillomavirus (HPV)

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49
Q

What other cancers is HPV associated ith

A

anal, vulval, vaginal, penis, mouth and throat cancers.

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50
Q

What two strains of HPV are responsible for 80% of cervical cancer cases

A

type 16 and 18

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51
Q

How does HPV promote the development of cancer

A

HPV produces two proteins (E6 and E7) that inhibit tumour suppressor genes

E6 protein inhibits p53

E7 protein inhibits pRb.

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52
Q

What are rick factors for cervical cancer

A

Early sexual activity
Increased number of sexual partners
Sexual partners who have had more partners
Not using condoms
Non-engagement with cervical screening
Smoking
HIV
Combined contraceptive pill >5 years
Increased number of full-term pregnancies
Family history

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53
Q

How does cervical cancer present

A

often detected asymptomatic

Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)
Vaginal discharge
Pelvic pain
Dyspareunia (pain or discomfort with sex)

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54
Q

How does cervical cancer appear on examination

A

Ulceration
Inflammation
Bleeding
Visible tumour

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55
Q

How are precursor to squamous cell carcinoma of the cervix graded

A

Cervical intraepithelial neoplasia (CIN)

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56
Q

how is Cervical intraepithelial neoplasia (CIN) diagosed

A

colposcopy

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57
Q

What does Cervical intraepithelial neoplasia (CIN) grade

A

dysplasia (premalignant change)

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58
Q

What does smear results show

A

dyskaryosis (precancerous changes)

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59
Q

What is CIN 1

A

mild dysplasia

affecting 1/3 the thickness of the epithelial layer

likely to return to normal without treatment

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60
Q

What is CIN 3

A

severe dysplasia

very likely to progress to cancer if untreated

sometimes called cervical carcinoma in situ.

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61
Q

What is CIN 2

A

moderate dysplasia

affecting 2/3 the thickness of the epithelial layer

likely to progress to cancer if untreated

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62
Q

how is cervical cancer screened

A

cervical smear test

precancerous changes in the epithelial cells of the cervix

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63
Q

how often do you have cervical screen

A

Every three years aged 25 – 49
Every five years aged 50 – 64

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64
Q

what are cervical smear samples tested for

A

Tested for high-risk HPV then the cells are examined.

If HPV negative then cell not tested

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65
Q

What women are exceptions to standard cervical screening program

A
  • Women with HIV (annually)
  • Women over 65 may request a smear if they have not had one since aged 50
  • Women with previous CIN may require additional tests (e.g. test of cure after treatment)
  • immunocompromised women may have additional screening (e.g. women on dialysis, cytotoxic drugs or undergoing an organ transplant)
  • Pregnant women due a routine smear should wait until 12 weeks post-partum
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66
Q

What other conditions can be identified on a smear test

A

bacterial vaginosis, candidiasis and trichomoniasis

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67
Q

What happens to women with HPV positive with abnormal cytology smear result

A

refer for colposcopy

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68
Q

What happens to women with HPV positive with normal cytology smear result

A

repeat the HPV test after 12 months

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69
Q

What is Colposcopy

A

Inserting a speculum and using equipment (a colposcope) to magnify the cervix.

stains such as acetic acid and iodine solution can be used to differentiate abnormal areas.

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70
Q

What does Acetic acid do in a colposcopy

A

causes abnormal cells to appear white
(acetowhite)

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71
Q

Why do abnormal cells turn white with acetic

A

increased nuclear to cytoplasmic ratio (more nuclear material)

such as cervical intraepithelial neoplasia and cervical cancer cells.

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72
Q

What is Schiller’s iodine test

A

an iodine solution to stain the cells of the cervix.

Iodine will stain healthy cells a brown colour.

Abnormal areas will not stain.

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73
Q

How are tissue samples collected in colposcopy

A

punch biopsy or large loop excision of the transformational zone

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74
Q

What is Large Loop Excision of the Transformation Zone (LLETZ)

A

using a loop of wire with electrical current (diathermy) to remove abnormal epithelial tissue on the cervix

Loop Biopsy

local anaesthetic

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75
Q

What is a cone biopsy

A

treatment for cervical intraepithelial neoplasia (CIN) and very early-stage cervical cancer.

surgeon removes a cone-shaped piece of the cervix using a scalpel

general anaesthetic

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76
Q

what are the risks of Cone Biopsy

A

Pain
Bleeding
Infection
Scar formation with stenosis of the cervix
Increased risk of miscarriage and premature labour

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77
Q

what are the risks of loop Biopsy

A

may increase the risk of preterm labour.
bleeding and abnormal discharge

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78
Q

how is cervical cancer staged

A

International Federation of Gynaecology and Obstetrics (FIGO

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79
Q

What are the stages of cervical cancer (stage 1-4)

A

Stage 1: Confined to the cervix
Stage 2: Invades the uterus or upper 2/3 of the vagina
Stage 3: Invades the pelvic wall or lower 1/3 of the vagina
Stage 4: Invades the bladder, rectum or beyond the pelvis

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80
Q

How is cervical intraepithelial neoplasia and early-stage 1A cervical cancer managed

A

gold standard = hysterectomy +/- lymph
node clearance

maintain fertility = LLETZ or cone biopsy
with negative margins

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81
Q

How is Stage 1B cervical cancer managed

A

Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy

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82
Q

How is Stage B2 cervical cancer managed

A

radical hysterectomy with pelvic lymph
node dissection

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83
Q

How is Stage 2 and 3 cervical cancer managed

A

radiation with concurrent
chemotherapy

if hydronephrosis → nephrostomy

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84
Q

How is Stage 4 cervical cancer managed

A

radiation and/or chemotherapy

4B = palliative chemotherapy

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85
Q

What monoclonal antibody is used in combo w chemo for metastatic or recurrent cervical cancer

A

Bevacizumab (Avastin)

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86
Q

What does Bevacizumab (Avastin) target

A

targets vascular endothelial growth factor A (VEGF-A)

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87
Q

What HPV strain cause genital warts

A

6 and 11

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88
Q

What is the 5 year survival for stage 1A cervical cancer

A

98%

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89
Q

What is the 5 year survival for stage 4 cervical cancer

A

15%

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90
Q

What is menorrhagia

A

Heavy menstrual bleeding

> 80ml loss

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91
Q

Name 5 causes of menorrhagia

A
  • Dysfunctional uterine bleeding (no identifiable cause)
  • Extremes of reproductive age
  • Fibroids
  • Endometriosis and adenomyosis
  • Pelvic inflammatory disease (infection)
  • Contraceptives, particularly the copper coil
  • Anticoagulant medications
  • Bleeding disorders (e.g. Von Willebrand disease)
  • Endocrine disorders (diabetes and hypothyroidism)
  • Connective tissue disorders
  • Endometrial hyperplasia or cancer
  • Polycystic ovarian syndrome
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92
Q

Name 5 key history questions to ask a woman presenting with menorrhagia

A
  • Age at menarche
  • Cycle length, days menstruating and variation
  • Intermenstrual bleeding and post coital bleeding
  • Contraceptive history
  • Sexual history
  • Possibility of pregnancy
  • Plans for future pregnancies
  • Cervical screening history
  • Migraines with or without aura (for the pill)
  • Past medical history and past drug history
  • Smoking and alcohol history
  • Family history
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93
Q

How should menorrhagia be investigated

A

Pelvic examination with a speculum and bimanual
FBC
Hysteroscopy
Pelvic and transvaginal ultrasound
Swabs
Coag screen
Ferritin
TFT

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94
Q

How is menorrhagia managed when the woman does not want contraception

A

Tranexamic acid when NO associated pain (antifibrinolytic – reduces bleeding)

Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

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95
Q

How is menorrhagia managed when the woman wants contraception

A
  1. Mirena coil (first line)
  2. Combined oral contraceptive pill
  3. Cyclical oral progestogens, such as norethisterone 5mg three times daily from day 5 – 26 (although this is associated with progestogenic side effects and an increased risk of venous thromboembolism)
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96
Q

What is the final option for when medical management has failed for menorrhagia

A

endometrial ablation and hysterectomy.

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97
Q

What is endometrial cancer

A

Cancer of the endometrium, the lining of the uterus.

80% of cases are adenocarcinoma

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98
Q

What is endometrial cancer dependent on

A

oestrogen-dependent cancer, meaning that oestrogen stimulates the growth of endometrial cancer cells.

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99
Q

What is the key presenting feature of endometrial cancer

A

a woman presenting with postmenopausal bleeding

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100
Q

What are risk factors for endometrial cancer

A

obesity and diabetes
PCOS
tamoxifen

excess oestrogen
- nulliparity
- early menarche
- late menopause
- unopposed oestrogen

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101
Q

what is endometrial hyperplasia

A

a precancerous condition involving thickening of the endometrium

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102
Q

What percent of cases of endometrial hyperplasia turn into endometrial cancer

A

5%

Most cases of endometrial hyperplasia will return to normal

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103
Q

Name the 2 types of endometrial hyperplasia

A

Hyperplasia without atypia
Atypical hyperplasia

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104
Q

How is endometrial hyperplasia without atypia treated

A

high dose progestogens with repeat sampling in 3-4 months (eg levonorgestrel intra-uterine system)

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105
Q

How is atypical endometrial hyperplasia treated

A

hysterectomy

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106
Q

How does unopposed oestrogen contribute to endometrial cancer

A

stimulates the endometrial cells and increases the risk of endometrial hyperplasia and cancer.

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107
Q

what is unopposed oestrogen

A

oestrogen without progesterone

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108
Q

Name causes of increased exposure of unopposed oestrogen

A

Increased age
Earlier onset of menstruation
Late menopause
Oestrogen only hormone replacement therapy
No or fewer pregnancies
Obesity
Polycystic ovarian syndrome
Tamoxifen

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109
Q

How does PCOS lead to increased exposure to unopposed oestrogen

A

lack of ovulation

less likely to form corpus luteum –> what produces progesterone & endometrial lining has more exposure to unopposed oestrogen

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110
Q

What should women with PCOS take for endometrial protection

A

The combined contraceptive pill
An intrauterine system (e.g. Mirena coil)
Cyclical progestogens to induce a withdrawal bleed.

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111
Q

How does obesity contribute to unopposed oestrogen

A

adipose tissue (fat) is a source of oestrogen

Adipose tissue is the primary source of oestrogen in postmenopausal women

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112
Q

What does adipose fat contain to contribute to unopposed oestrogen and what does it do

A

aromatase, which is an enzyme that converts androgens such as testosterone into oestrogen

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113
Q

What is tamoxifen oestrogenic effect

A

anti-oestrogenic effect on breast tissue, but an oestrogenic effect on the endometrium.

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114
Q

name two risk factors for endometrial cancer not related to unopposed oestrogen

A

Type 2 diabetes
Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome

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115
Q

name 4 protective factors against endometrial cancer

A

Combined contraceptive pill
Mirena coil
Increased pregnancies
Cigarette smoking

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116
Q

How may endometrial cancer present

A

** postmenopausal bleeding **

also

Postcoital bleeding
Intermenstrual bleeding
Unusually heavy menstrual bleeding
Abnormal vaginal discharge
Haematuria
Anaemia
Raised platelet count

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117
Q

What is the referral criteria for a 2 week wait for endometrial cancer

A

Postmenopausal bleeding (more than 12 months after the last menstrual period)

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118
Q

What is the NICE criteria for referral for a transvaginal ultrasound with suspected endometrial caner

A

women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway

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119
Q

What are the three investigations for endometrial cancer

A

Transvaginal ultrasound for endometrial thickness
hysteroscopy with endometrial biopsy

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120
Q

What is a normal endometrial thickness post menopause

A

less than 4mm

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121
Q

What is a pipelle biopsy

A

highly sensitive for endometrial cancer

inserting thin tube (pipelle) through the cervix into the uterus

quicker and less invasive alternative than hysteroscopy

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122
Q

What indicated on investigations are sufficient to demonstrate a very low risk of endometrial cancer and discharge the patient.

A

a normal transvaginal ultrasound (endometrial thickness < 4mm) and normal pipelle biopsy

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123
Q

How is endometrial cancer staged

A

International Federation of Gynaecology and Obstetrics (FIGO) staging system

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124
Q

what are the International Federation of Gynaecology and Obstetrics (FIGO) staging system for endometrial cancer

A

Stage 1: Confined to the uterus
Stage 2: Invades the cervix
Stage 3: Invades the ovaries, fallopian tubes, vagina or lymph nodes
Stage 4: Invades bladder, rectum or beyond the pelvis

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125
Q

How is stage 1&2 endometrial cancer managed

A

total abdominal hysterectomy with bilateral salpingo-oophorectomy, also known as a TAH and BSO (removal of uterus, cervix and adnexa).

+/- radiotherapy

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126
Q

What is endometriosis

A

ectopic endometrial tissue outside the uterus
affects 10%

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127
Q

What are chocolate cysts

A

Endometriomas in the ovaries

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128
Q

What is Endometriomas

A

lump of endometrial tissue outside the uterus

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129
Q

What is Adenomyosis

A

endometrial tissue within the myometrium (muscle layer) of the uterus.

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130
Q

What is a theory for the cause of endometriosis

A

During menstruation, the endometrial lining flows backwards, through the fallopian tubes and out into the pelvis and peritoneum (retrograde menstruation)

The endometrial tissue then seeds itself around the pelvis and peritoneal cavity.

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131
Q

How does endometriosis present

A

Cyclical abdominal or pelvic pain
Deep dyspareunia (pain on deep sexual intercourse)
Dysmenorrhoea (painful periods - often before period starts)
Infertility
Cyclical bleeding from other sites, such as haematuria
urinary symptom
painful bowel movements

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132
Q

What can endometriosis in bladder and bowel cause

A

can lead to blood in the urine or stools.

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133
Q

How does endometriosis present on examination

A
  • Endometrial tissue visible particularly in the posterior fornix
  • reduced organ mobility
  • A fixed cervix on bimanual examination
  • Tenderness in the vagina, cervix and adnexa
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134
Q

What is the gold standard investigation for endometriosis?

A

Laparoscopic surgery

definitive diagnosis can be established with a biopsy of the lesions during laparoscopy.

1st = US

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135
Q

other than lapsroscopic surgery how else can endometriosis be investigated

A

Pelvic ultrasound

may reveal large endometriomas and chocolate cysts

however ultrasound are often unremarkable in patients with endometriosis

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136
Q

What is the body responsible for the staging system for endometriosis

A

American Society of Reproductive Medicine (ASRM)

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137
Q

what are the endometriosis stages (stage 1-4)

A

Stage 1: Small superficial lesions
Stage 2: Mild, but deeper lesions than stage 1
Stage 3: Deeper lesions, with lesions on the ovaries and mild adhesions
Stage 4: Deep and large lesions affecting the ovaries with extensive adhesions

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138
Q

What is the initial management of endometriosis

A

Establishing a diagnosis
Providing a clear explanation
Listening to the patient, establishing their ideas, concerns and expectations and building a partnership
Analgesia as required for pain (NSAIDs and paracetamol first line)

139
Q

What is the hormonal management of endometriosis

A

Combined oral contractive pill, which can be used back to back without a pill-free period if helpful
Progesterone only pill
Medroxyprogesterone acetate injection (e.g. Depo-Provera)
Nexplanon implant
Mirena coil
GnRH agonists

140
Q

What is the surgical management of endometriosis

A

Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)
Hysterectomy

141
Q

do hormonal therapies improve fertility in endometriosis

A

Hormonal therapies may improve symptoms but not fertility.

Laparoscopic treatment may improve fertility

142
Q

how does birth control medication manage endometriosis cyclical pain

A

stop ovulation and reduce endometrial thickening

143
Q

outside of uterus where can endometriosis be found

A

intestinal tract
bladder
heart
lungs
kidney
CNS

144
Q

how does GnRH agonists manage endometriosis cyclical pain

A

eg Goserelin

Cyclical pain tends to improve after menopause when the female sex hormones are reduced.

GnRH agonists induce a menopause-like state

Shut down the ovaries temporarily and can be useful in treating pain in many women

145
Q

How does laproscopic sugery improve endometriosis symptoms

A

excise or ablate the ectopic endometrial tissue. remove adhesions causing chronic pelvic pain

146
Q

What is the final surgical option for endometriosis

A

Hysterectomy and bilateral salpingo-opherectomy

147
Q

What are fibriods

A

benign tumours of the smooth muscle of the uterus

148
Q

What is another name for fibriods

A

uterine leiomyomas

149
Q

How many women are affected by fibrioids

A

40-60% of women in later reproductive years
more common in black women

150
Q

What hormone are fibroids sensitive to

A

oestrogen

151
Q

What are 4 types of fibroids

A

Intramural
Subserosal
Submucosal
Pedunculated

152
Q

What are intramural fibroids

A

within the myometrium (the muscle of the uterus

As they grow, they change the shape and distort the uterus.

153
Q

What are Subserosal fibroids

A

just below the outer layer of the uterus

grow outwards and can become very large, filling the abdominal cavity

154
Q

What are Submucosal fibroids

A

just below the lining of the uterus (the endometrium)

155
Q

What are Pedunculated fibroids

A

on a stalk

156
Q

How do fibroids present

A
  • Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom
  • Prolonged menstruation, lasting more than 7 days
  • Abdominal pain, worse during menstruation
  • Bloating or feeling full in the abdomen
  • Urinary or bowel symptoms due to pelvic pressure or fullness
  • Deep dyspareunia (pain during intercourse)
  • Reduced fertility
157
Q

How do fibroids present one examination

A

may reveal a palpable pelvic mass or an enlarged firm non-tender uterus.

158
Q

What is the first line investigation for fibroids

A

transvaginal and transabdominal ultrasound

159
Q

What is the 1st line medical management for fibroids

A

Mirena coil (1st line) – fibroids must be less than 3cm with no distortion of the uterus

Symptomatic management with NSAIDs and tranexamic acid

160
Q

What is the surgical management for fibroids if fertility desired

A
  • myomectomy
161
Q

what is the surgical management of fibroids if fertility not desired

A

Uterine artery embolisation
Hysterectomy

162
Q

What is Uterine artery embolisation

A

Inserts a catheter into femoral artery & passed through to the uterine artery under X-ray

Once in the correct place, particles are injected that cause a blockage in the arterial supply to the fibroid.

This starves the fibroid of oxygen and causes it to shrink

163
Q

What is myomectomy

A

surgically removing the fibroid via laparoscopic (keyhole) surgery or laparotomy (open surgery).

only treatment known to potentially improve fertility

164
Q

What are complications of fibroids

A
  • Heavy menstrual bleeding, often with iron deficiency anaemia
  • Reduced fertility
  • Pregnancy complications, such as miscarriages, premature labour and obstructive delivery
  • Constipation
  • Urinary outflow obstruction and urinary tract infections
  • Red degeneration of the fibroid
  • Torsion of the fibroid, usually affecting pedunculated fibroids
  • Malignant change to a leiomyosarcoma is very rare (<1%)
165
Q

What is red degeneration of fibroids

A

ischaemia, infarction and necrosis of the fibroid due to fibroid outgrowing its blood supply

more likely to occur in larger fibroids (above 5 cm) during the second and third trimester of pregnancy.

166
Q

How does a woman with red degeneration of fibroids present

A

pregnant woman with a history of fibroids presenting with severe abdominal pain and a low-grade fever

maybe tachycardia and vomiting

167
Q

What is a hydatiform mole

A

A type of tumour that grows like a pregnancy inside the uterus. This is called a molar pregnancy

168
Q

what is a complete mole

A

when two sperm cells fertilise an ovum that contains no genetic material (an “empty ovum”).

These sperm then combine genetic material, and the cells start to divide and grow into a tumour called a complete mole.

No fetal material will form

169
Q

What is a partial mole

A

when two sperm cells fertilise a normal ovum (containing genetic material) at the same time.

The new cell now has three sets of chromosomes. The cell divides and multiplies into a tumour called a partial mole.

some fetal material may form.

170
Q

What indicates a molar pregnancy vs a normal pregnancy

A

More severe morning sickness
Vaginal bleeding
Increased enlargement of the uterus
Abnormally high hCG
Thyrotoxicosis (hCG can mimic TSH and stimulate the thyroid to produce excess T3 and T4)

171
Q

How does molar pregnancy present on ultrasound

A

“snowstorm appearance” of the pregnanc

172
Q

How is a molar pregnancy diagnosed

A

Ultrasound of the pelvis

Provisional diagnosis can be made by ultrasound and confirmed with histology of the mole after evacuation.

173
Q

How is a molar pregnancy managed

A

evacuation of the uterus to remove the mole & sent for histological examination

referred to the gestational trophoblastic disease centre

hCG levels monitored

174
Q

What is the management for a metastatic molar pregnancy

A

systemic chemotherapy

175
Q

What is lichen sclerosus

A

chronic inflammatory skin condition
commonly affecrs the labia perineum and perianal skin
autoimmune condition

176
Q

what does lichen mean

A

flat eruption that spreads

177
Q

how does lichen sclerosus present

A

45-60 year old woman complaining of vulval itching and skin changes in the vulva

skin tightness
painful sex
erosions
fissures

patches of shiny, “porcelain-white” skin

178
Q

What is the koebner phenomenon

A

when the signs and symptoms are made worse by friction to the skin

occurs with lichen sclerosus or psoriasis

179
Q

How does lichen sclerosus appear

A

“Porcelain-white” in colour
Shiny
Tight
Thin
Slightly raised
There may be papules or plaques

180
Q

How is lichen sclerosus managed

A

cannot be cured, but the symptoms can be effectively controlled.

topical steroids and emollients –> clobetasol propionate 0.05% (dermovate).

181
Q

What is a critical complication of lichen sclerosus

A

5% risk of developing squamous cell carcinoma of the vulva.

182
Q

What conditions is lichen sclerosus associated with

A

type 1 diabetes, alopecia, hypothyroid and vitiligo.

183
Q

What is menarche

A

The age at onset of menstrual bleeding. Mean age is 13 years; typically occurs 2 years after the onset of puberty.

184
Q

What is menopause

A

permanent stop to menstruation

185
Q

How is menopause diagnosed

A

retrospective diagnosis

made after a woman has had no periods for 12 months

NICE recomends FSH blood test

186
Q

What is post menopause

A

the period from 12 months after the final menstrual period onwards.

187
Q

what is perimenopause

A

time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods

188
Q

What is premature menopause

A

menopause before the age of 40 years

189
Q

What causes premature menopause

A

premature ovarian insufficiency

190
Q

What is cause of menopause

A

lack of ovarian follicular function,

191
Q

How do sex hormones change in menopause

A

Oestrogen and progesterone levels are low
LH and FSH levels are high, in response to an absence of negative feedback from oestrogen

192
Q

What are the perimenopausal symptoms

A

Hot flushes
Emotional lability or low mood
Premenstrual syndrome
Irregular periods
Joint pains
Heavier or lighter periods
Vaginal dryness and atrophy
Reduced libido

193
Q

what are the risks of lack of oestrogen

A

Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

194
Q

How long do women need to use contraception after last menstraul period

A

<50 = 2 years after last period
>50 = 1 year after last period

195
Q

What are good contraceptive options (UKMEC 1, meaning no restrictions) for women approaching the menopause

A

Barrier methods
Mirena or copper coil
Progesterone only pill
Progesterone implant
Progesterone depot injection (under 45 years)
Sterilisation

196
Q

What is a UKMEC 2 (the advantages generally outweigh the risks) contraception

A

combined oral contraceptive pill

197
Q

What are the two key side effects of the progesterone depot injection

A

weight gain and reduced bone mineral density (osteoporosis).

198
Q

How are perimenopausal symptoms managed

A
  • No treatment
  • Hormone replacement therapy (HRT)
  • Tibolone, a synthetic steroid hormone that acts as continuous combined HRT
  • Testosterone
  • CBT
  • SSRI
199
Q

What is ovarian cancer

A

cancer of the ovaries
non specific symptoms
More than 70% of patients with ovarian cancer present after it has spread beyond the pelvis.

200
Q

What is the most common type of ovarian cancer

A

Epithelial cell tumours

201
Q

Name 3 subtypes of epithelial cell tumours

A
  • Serous tumours (the most common)
  • Endometrioid carcinomas
  • Clear cell tumours
  • Mucinous tumours
  • Undifferentiated tumours
202
Q

what is a teratoma

A

benign ovarian tumours
arise from germ cells

203
Q

what markers can germ cell tumors raise

A

alpha-fetoprotein (α-FP)
human chorionic gonadotrophin (hCG)

204
Q

What other condition are germ cell tumors associated with

A

ovarian torsion

205
Q

Where do Sex Cord-Stromal Tumours arsie from

A

stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)

benign or malignant

206
Q

Name two types of Sex Cord-Stromal Tumours

A

Sertoli–Leydig cell tumours and granulosa cell tumours.

207
Q

What is a krukenberg tumor

A

metastasis in the ovary from GI tract cancer

208
Q

What is the characteristic sign on histology for krukenberg tumor

A

“signet-ring” cells

209
Q

What are risk factors for ovarian cancer

A
  • Age (peaks age 60)
  • BRCA1 and BRCA2 genes (consider the family history)
  • Increased number of ovulations
  • Early-onset of periods
  • Late menopause
  • No pregnancies
  • Obesity
  • Smoking
  • Recurrent use of clomifene
  • Tamoxifen
210
Q

What are protective factors for ovarian cancer

A

Combined contraceptive pill
Breastfeeding
Pregnancy

(factors that reduce ovulations)

211
Q

How does ovarian cancer present

A

non-specific symptoms

Abdominal bloating
Early satiety (feeling full after eating)
Loss of appetite
Abdominal or pelvic mass
Urinary symptoms (frequency / urgency)
Weight loss
Ascites

212
Q

Where can ovarian cancer cause referred pain

A

may press on the obturator nerve and cause referred hip or groin pain

213
Q

What is the criteria for two week wait for suspected ovarian cancer

A

Ascites
Pelvic mass (unless clearly due to fibroids)
Abdominal mass

214
Q

What symptoms indicated further investigation before cancer referral in women presenting with symptoms of possible ovarian cancer

A

women >50

New symptoms of IBS / change in bowel habit
Abdominal bloating
Early satiety
Pelvic pain
Urinary frequency or urgency
Weight loss

215
Q

What are the initial investigations for ovarian cancer in primary or secondary care

A

CA125 blood test (>35 IU/mL is significant)
Pelvic ultrasound

216
Q

What is included in the risk of malignancy index (RMI) for ovarian cancer

A

Menopausal status
Ultrasound findings
CA125 level

217
Q

What further investigations can be done in secondary care for ovarian cancer

A
  • CT scan to establish the diagnosis and stage the cancer
  • Histology (tissue sample) using a CT guided biopsy, laparoscopy or laparotomy
  • Paracentesis (ascitic tap) can be used to test the ascitic fluid for cancer cells
218
Q

What tumor marker tests are required for women under 40 with complex ovarian mass and why

A

Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)
Lactate dehydrogenase (LDH)

for possible germ cell tumor

219
Q

what is CA125 a tumor marker for

A

epithelial cell ovarian cancer

220
Q

What are non malignant causes for raised CA125

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

221
Q

What are the stages for ovarian caner

A

International Federation of Gynaecology and Obstetrics (FIGO) staging system

Stage 1: Confined to the ovary
Stage 2: Spread past the ovary but inside the pelvis
Stage 3: Spread past the pelvis but inside the abdomen
Stage 4: Spread outside the abdomen (distant metastasis)

222
Q

how is ovarian cancer managed

A

specialist gynaecology oncology MDT. It usually involves a combination of surgery and chemotherapy.

223
Q

What is an cyst

A

fluid-filled sac

224
Q

What is a functional ovarian cysts

A

An ovarian cyst that develops due to disruption in the development of follicles or the corpus luteum.

related to the fluctuating hormones of the menstrual cycle

very common in premenopausal

follicular or corpus luteum

225
Q

At what age are ovarian cysts more concerning

A

Cysts in postmenopausal women are more concerning for malignancy

226
Q

How do ovarian cysts present

A

Most ovarian cysts are asymptomatic

Occasionally, ovarian cysts can cause vague symptoms of:

Pelvic pain
Bloating
Fullness in the abdomen
A palpable pelvic mass (particularly with very large cysts such as mucinous cystadenomas)

227
Q

When may ovarian cysts present with acute pain

A

if there is ovarian torsion, haemorrhage or rupture of the cyst.

228
Q

What are the most common ovarian cyst

A

Follicular cysts

229
Q

What are Follicular cysts

A

Developing follicle fail to rupture and release the egg (ovulate), the cyst can persist

may produce excess oestrogen

tend to disappear after a few menstrual cycles

230
Q

What is a Corpus luteum cysts

A

occur when the corpus luteum fails to break down (involute) and instead fills with fluid.

may produce excess progesterone

often seen in early pregnancy.

231
Q

Name three other types of ovarian cysts

A

Serous Cystadenoma
Mucinous Cystadenoma
Endometrioma
Dermoid Cysts / Germ Cell Tumours
Sex Cord-Stromal Tumours

232
Q

what cysts are benign tumors of epithelial cells

A

Serous Cystadenoma
Mucinous Cystadenoma

233
Q

What are endometrioma

A

lumps of endometrial tissue within the ovary, occurring in patients with endometriosis. They can cause pain and disrupt ovulation.

234
Q

What features of ovaian cysts may suggest malignancy

A

Abdominal bloating
Reduce appetite
Early satiety
Weight loss
Urinary symptoms
Pain
Ascites
Lymphadenopathy

235
Q

What is the tumor marker for ovarian cancer

A

CA 125

236
Q

What is the name of the guidline for managing suspected ovarian cysts

A

RCOG Green-top guidelines

237
Q

What is the referral for possible ovarian cancer (complex cysts or raised CA125)

A

two-week wait referral to a gynaecological oncology specialist.

238
Q

What is the referral for possible dermoid cysts

A

referral to a gynaecologist for further investigation and consideration of surgery.

239
Q

What is the management for premenopausal women with a ovarian cyst <5cm

A

almost always resolve within three cycles.

A repeat ultrasound should be arranged for 8-12 weeks

240
Q

What is the management for premenopausal women with a ovarian cyst 5cm to 7cm

A

Require routine referral to gynaecology and yearly ultrasound monitoring.

241
Q

What is the management for premenopausal women with a ovarian cyst >7cm

A

Consider an MRI scan or surgical evaluation as they can be difficult to characterise with ultrasound.

242
Q

What is the management for cysts in postmenopausal women

A

benign unlikely in post menopausal women –> any postmenopausal woman with an ovarian cyst regardless of nature or size should be referred to gynaecology for assessment

243
Q

How are persistent or enlarging cysts managed

A

surgical intervention (usually with laparoscopy)

involve removing the cyst (ovarian cystectomy), possibly along with the affected ovary (oophorectomy).

244
Q

What are the complication of ovarian cysts

A

Torsion
Haemorrhage into the cyst
Rupture, with bleeding into the peritoneum

245
Q

What is Meigs syndrome

A

triad:
Ovarian fibroma (a type of benign ovarian tumour)
Pleural effusion
Ascites

246
Q

What is ovarian torsion

A

ovary twists in relation to the surrounding connective tissue, fallopian tube and blood supply (the adnexa).

247
Q

What are the RF of ovarian torsion

A
  • ovarian mass >5cm such as cyst or tumor
  • pregnancy
  • longer infundibulopelvic ligaments
248
Q

What happens with twisting of the adnexa in ovarian torsion

A

Twisting of the adnexa and blood supply to the ovary leads to ischaemia

If the torsion persists, necrosis will occur, and the function of that ovary will be lost

249
Q

How does ovarian torsion present

A

sudden onset severe unilateral pelvic pain
constant pain
progressive pain
nausea and vomiting

250
Q

What initial investigation for ovarian torsion

A

Pelvic ultrasound
Transvaginal is ideal, but transabdominal can be used

251
Q

What is the ultrasound sign for ovarian torsion

A

“whirlpool sign”, free fluid in pelvis and oedema of the ovary.

252
Q

What investigation is used for definitive diagnosis of ovarian torsion

A

laparoscopic surgery

253
Q

How is ovarian torsion managed

A

laparoscopic surgery to
- un-twist the ovary and fix it in place (detorsion)
- Remove the affected ovary (oophorectomy)

254
Q

What is complication of ovarian torsion

A

loss of function of that ovary
fertility is not typically affected if there is another ovary

255
Q

What can a necrotic ovarian lead to

A

become infected, develop an abscess and lead to sepsis.

may rupture, resulting in peritonitis and adhesions.

256
Q

What are characterisitc features of PCOS

A
  • multiple ovarian cysts
  • oligomenorrhea
  • hyperandrogenism
  • infertility
  • insulin resistance.
257
Q

What is Anovulation

A

absence of ovulation

258
Q

What is Oligoovulation

A

irregular, infrequent ovulation

259
Q

what is Amenorrhoea

A

absence of menstrual periods

260
Q

what is Oligomenorrhoea

A

irregular, infrequent menstrual periods

261
Q

what are Androgens

A

male sex hormones, such as testosterone

262
Q

What is Hyperandrogenism

A

effects of high levels of androgens

263
Q

what is Hirsutism

A

growth of thick dark hair, often in a male pattern, for example, male pattern facial hair

264
Q

What is Insulin resistance

A

lack of response to the hormone insulin, resulting in high blood sugar levels

265
Q

What criteria is used to making a diagnosis of PCOS

A

Rotterdam criteria

266
Q

What is Rotterdam criteria

A

2/3

infrequent or no ovulation
hyperandrogenism
polycystic ovaries on ultrasound ≥ 12 follicles

267
Q

What are key features of PCOS presentation

A

Oligomenorrhoea or amenorrhoea
Infertility
Obesity (in about 70% of patients with PCOS)
Hirsutism
Acne
Hair loss in a male pattern

268
Q

What are other features and complications of PCOS

A
  • Insulin resistance and diabetes
  • Acanthosis nigricans
  • Cardiovascular disease
  • Hypercholesterolaemia
  • Endometrial hyperplasia and cancer
  • Obstructive sleep apnoea
  • Depression and anxiety
  • Sexual problems
269
Q

What are differential diagnosis of hirsutism

A
  • Medications, such as phenytoin, ciclosporin, corticosteroids, testosterone and anabolic steroids
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • Congenital adrenal hyperplasia
270
Q

What happened when someone is resistant to insulin in PCOS

A

Pancreas has to produce more insulin to get response
High Insulin =

  • promotes the release of androgens
  • suppresses sex hormone-binding globulin (SHBG) promoting hyperandrogenism
  • halt the development of the follicles in the ovaries, leading to anovulation
271
Q

What lifestyle management can help reduce insulin resistance

A

Diet, exercise and weight loss

272
Q

What blood tests are recommended to diagnose PCOS

A

Testosterone
Sex hormone-binding globulin
Luteinizing hormone
Follicle-stimulating hormone
Prolactin (may be mildly elevated in PCOS)
Thyroid-stimulating hormone

273
Q

What do hormone blood test typically show for PCOS

A

Raised luteinising hormone **
Raised LH to FSH ratio (high LH compared with FSH) ***

Raised testosterone
Raised insulin
Normal or raised oestrogen levels

274
Q

What is the gold standard investigation for visualising the ovaries in PCOS

A

transvaginal ultrasound

275
Q

What is the diagnostic criteria for PCOS on ultrasound

A

either:
- 12 or more developing follicles in one ovary
- Ovarian volume of more than 10cm3

276
Q

What is the sign on ultrasound for PCOS

A

“string of pearls” appearance.

277
Q

What is the screening test of choice for diabetes in patients with PCOS

A

2-hour 75g oral glucose tolerance test (OGTT).

taking a baseline fasting plasma glucose, giving a 75g glucose drink and then measuring plasma glucose 2 hours later.

278
Q

What are potential results from oral glucose tolerance test (OGTT)

A
  • Impaired fasting glucose – fasting glucose of 6.1 – 6.9 mmol/l (before the glucose drink)
  • Impaired glucose tolerance – plasma glucose at 2 hours of 7.8 – 11.1 mmol/l
  • Diabetes – plasma glucose at 2 hours above 11.1 mmol/l
279
Q

What is the cut off from impaired glucose tolerance and diabetes

A

plasma glucose >11.1mmol/l

280
Q

What medical conditions are associated with PCOS

A

obesity
type 2 diabetes
hypercholesterolaemia
cardiovascular disease

281
Q

What are the lifestyle changes used to reduce risk of medical conditions associated with PCOS

A

Weight loss
Low glycaemic index, calorie-controlled diet
Exercise
Smoking cessation
Antihypertensive medications where required
Statins where indicated (QRISK >10%)

282
Q

What are complications of PCOS

A

Endometrial hyperplasia and cancer
Infertility
Hirsutism
Acne
Obstructive sleep apnoea
Depression and anxiety

283
Q

What medication may be used to help weight loss in women with BMI >30 with PCOD

A

Orlistat - lipase inhibitor
stops the absorption of fat in the intestines.

284
Q

What are the benefits of weight loss in PCOS

A
  • ovulation and restore fertility and regular menstruation
  • improve insulin resistance
  • reduce hirsutism
  • reduce the risks of associated conditions
285
Q

why are women with PCOS at increased risk of endometrial cancer

A
  • PCOS ovulate infrequently -> do not produce sufficient progesterone
  • do not experience regular menstruation
  • endometrial lining continues to proliferate under the influence of oestrogen, without regular shedding

similar to unopposed oestrogen

286
Q

what is the management for reducing the risk of endometrial hyperplasia and endometrial cancer in women with PCOS

A

Mirena coil for continuous endometrial protection
Inducing a withdrawal bleed with either combined pill or cyclical progestogen

287
Q

How do women with extended gaps between periods (more than three months) or abnormal bleeding need to be investigated

A

pelvic ultrasound to assess the endometrial thickness

Cyclical progestogens should be used to induce a period prior to the ultrasound scan.
If the endometrial thickness is more than 10mm, they need to be referred for a biopsy to exclude endometrial hyperplasia or cancer.

288
Q

What is the inital step for improving fertility in PCOS

A

weight loss

289
Q

When weight loss fails to restore fertility for PCOS what is next step

A

Clomifene
Laparoscopic ovarian drilling
In vitro fertilisation (IVF)

290
Q

What is Ovarian drilling

A

laparoscopic surgery. The surgeon punctures multiple holes in the ovaries using diathermy or laser therapy.

can improve the woman’s hormonal profile and result in regular ovulation and fertility.

291
Q

What must women with PCOD must be screened for in pregnancy

A

gestational diabetes

oral glucose tolerance test, performed before pregnancy and at 24 – 28 weeks gestation.

292
Q

Hwo is hirsutism managed

A

weight loss
Co-cyprindiol (Dianette) - COCP - anti-androgenic effect
Topical eflornithine

293
Q

What is a side effect of Co-cyprindiol (Dianette)

A

venous thromboembolism.

294
Q

What is 1st line management for acne in PCOS

A

combined oral contraceptive pill

295
Q

What are other management options for ance

A

Topical adapalene (a retinoid)
Topical antibiotics (e.g. clindamycin 1% with benzoyl peroxide 5%)
Topical azelaic acid 20%
Oral tetracycline antibiotics (e.g. lymecycline)

296
Q

What is pelvic inflammatory disease

A

inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix.

It is a significant cause of tubular infertility and chronic pelvic pain.

297
Q

What is Salpingitis

A

inflammation of the fallopian tubes

298
Q

what is Oophoritis

A

inflammation of the ovaries

299
Q

What is Parametritis

A

inflammation of the parametrium, which is the connective tissue around the uterus

300
Q

What is Peritonitis

A

inflammation of the peritoneal membrane

301
Q

What are sexually transmitted causes of PID

A

Neisseria gonorrhoeae tends to produce more severe PID
Chlamydia trachomatis
Mycoplasma genitalium

302
Q

what are non sexually transmitted causes of PID

A
  • Gardnerella vaginalis (associated with bacterial vaginosis)
  • Haemophilus influenzae (a bacteria often associated with respiratory infections)
  • Escherichia coli (an enteric bacteria commonly associated with urinary tract infections
303
Q

What are the risk factors of PID

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)

304
Q

What are the examination findings of PID

A

Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge

may have a fever and other signs of sepsis.

305
Q

How does PID present

A

Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria

306
Q

How is PID investiagted

A

NAAT swabs for gonorrhoea and chlamydia
NAAT swabs for Mycoplasma genitalium if available
HIV test
Syphilis test

A high vaginal swab can be used to look for bacterial vaginosis, candidiasis and trichomoniasis.

307
Q

What test should be preformed on sexually active women presenting with lower abdominal pain

A

pregnancy test to exclude an ectopic pregnancy.

308
Q

What empirical antibiotics are started for PID to cover gonorrhoea

A

single dose IM ceftriaxone 1g

309
Q

What empirical antibiotics are started for PID to cover hlamydia and Mycoplasma genitalium

A

Doxycycline 100mg twice daily for 14 days

310
Q

What empirical antibiotics are started for PID to cover anaerobes such as Gardnerella vaginalis

A

Metronidazole 400mg twice daily for 14 days

311
Q

What are complications of PID

A

Sepsis
Abscess
Infertility
Chronic pelvic pain
Ectopic pregnancy
Fitz-Hugh-Curtis syndrome

312
Q

What is Fitz-Hugh-Curtis Syndrome

A

caused by inflammation and infection of the liver capsule (Glisson’s capsule), leading to adhesions between the liver and peritoneum. Bacteria may spread from the pelvis via the peritoneal cavity, lymphatic system or blood.

313
Q

how does Fitz-Hugh-Curtis Syndrome present

A

right upper quadrant pain that can be referred to the right shoulder tip if there is diaphragmatic irritation

314
Q

What is Galactorrhoea

A

breast milk production not associated with pregnancy or breastfeeding.

Breast milk is produced in response to the hormone prolactin

315
Q

What is prolactinoma

A

hormone-secreting pituitary tumours secrete excessive prolactin

316
Q

How does hyperprolactinaemia present

A

Menstrual irregularities, particularly amenorrhoea (absent periods)
Reduced libido (low sex drive)
Erectile dysfunction (in men)
Gynaecomastia (in men)

317
Q

What would hormone test show for hyperprolactinaemia

A

Prolactin suppresses gonadotropin-releasing hormone (GnRH)

reduced LH and FSH release

318
Q

What conditions is associated with Prolactinomas

A

multiple endocrine neoplasia (MEN) type 1, an autosomal dominant genetic condition.

319
Q

What are thw two types of prolactiomas

A

Microprolactinomas – smaller than 10 mm
Macroprolactinomas – larger than 10 mm

320
Q

What are adverse effects of Macroprolactinomas

A

Headaches
Bitemporal hemianopia (loss of the outer visual fields in both eyes)

321
Q

how is prolactioma investigated

A

Serum prolactin
Renal profile (U&Es)
Liver function tests (LFTs)
Thyroid function tests (TFTs)

322
Q

How is prolactioma diagnosed

A

MRI scan for pituitary tumors

323
Q

How are prolactioma symptoms managed

A

Dopamine agonists (e.g., bromocriptine or cabergoline) –> block prolactin secretion and improve symptoms.

324
Q

What is the definitive management of prolactiomas

A

Trans-sphenoidal surgical removal of the pituitary tumour

325
Q

what is vulval cancer

A

rare
90% are squamous cell carcinomas.
Less commonly, they can be malignant melanomas.

326
Q

What are risk factors of vulval cancer

A

Lichen sclerosus (5% will get vulval cancer)
Advanced age (particularly over 75 years)
Immunosuppression
Human papillomavirus (HPV) infection

327
Q

What condition can precede vulval cancer

A

Vulval intraepithelial neoplasia (VIN)

328
Q

What Vulval intraepithelial neoplasia (VIN) is associated with HPV

A

High grade squamous intraepithelial lesion - 35 – 50 years.

329
Q

What Vulval intraepithelial neoplasia (VIN) is associated with lichen sclerosus

A

Differentiated VIN (aged 50 – 60 years).

330
Q

How is Vulval intraepithelial neoplasia (VIN) diagnosed

A

biopsy

331
Q

How is Vulval intraepithelial neoplasia (VIN) managed

A

Watch and wait with close followup
Wide local excision (surgery) to remove the lesion
Imiquimod cream
Laser ablation

332
Q

How does vulval cancer present

A

Vulval lump
Ulceration
Bleeding
Pain
Itching
Lymphadenopathy in the groin

333
Q

How does labia majora appear in vulval cancer

A

Irregular mass
Fungating lesion
Ulceration
Bleeding

334
Q

How is vulval cancer diagnses and staged

A

Biopsy of the lesion
Sentinel node biopsy to demonstrate lymph node spread
Further imaging for staging (e.g. CT abdomen and pelvis)

335
Q

What system is used to stage vulval cancer

A

International Federation of Gynaecology and Obstetrics (FIGO)

336
Q

How is vulval cancer managed

A

Wide local excision to remove the cancer
Groin lymph node dissection
Chemotherapy
Radiotherapy

337
Q

what is vaginal cancer

A

usually secondary to cervical SCC
primary to vaginal carcinoma rare

338
Q

What is Tanner stage 1

A

Under 10

No pubic hair

No Breast Development

339
Q

What is Tanner stage 2

A

10 – 11

Light and thin pubic hair

Breast buds form behind the areola

340
Q

What is Tanner stage 3

A

11 – 13

Course and curly pubic hair

Breast begins to elevate beyond the areola

341
Q

What is Tanner stage 4

A

13 – 14

Adult like but not reaching the thigh pubic hair

Areolar mound forms and projects from surrounding breast

342
Q

What is Tanner stage 5

A

Above 14

Hair extending to the medial thigh pubic hair

Areolar mounds reduce, and adult breasts form

343
Q

what are causes of primary amenorrhoea

A
  • gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes (RAISED LH/FSH)
  • testicular feminisation
  • congenital malformations of the genital tract
  • functional hypothalamic amenorrhoea (e.g. secondary to anorexia)
  • congenital adrenal hyperplasia
  • imperforate hymen
344
Q

what are causes of secondary amenorrhoea

A
  • hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)
  • polycystic ovarian syndrome (PCOS)
  • hyperprolactinaemia
  • premature ovarian failure
  • thyrotoxicosis*
  • Sheehan’s syndrome
  • Asherman’s syndrome (intrauterine adhesions

3a womens health (5 decks)

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