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Phase 3A > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

Differentials for primary amenorrhoea?

A

Abnormal functioning of the hypothalamus or pituitary gland (hypogonadotropic hypogonadism)
Abnormal functioning of the gonads (hypergonadotropic hypogonadism)
Imperforate hymen or other structural pathology

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2
Q

Differentials for pruritis vulvae?

A

Irritants such as soaps, detergents and barrier contraception
Atrophic vaginitis
Infections such as candidiasis (thrush) and pubic lice
Skin conditions such as eczema
Vulval malignancy
Pregnancy-related vaginal discharge
Urinary or faecal incontinence
Stress

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3
Q

Differentials for secondary amenorrhoea?

A

Pregnancy (the most common cause)
Menopause
Physiological stress due to excessive exercise, low body weight, chronic disease or psychosocial factors
Polycystic ovarian syndrome
Medications, such as hormonal contraceptives
Premature ovarian insufficiency (menopause before 40 years)
Thyroid hormone abnormalities (hyper or hypothyroid)
Excessive prolactin, from a prolactinoma
Cushing’s syndrome

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4
Q

Differentials for intermenstrual bleeding?

A

Hormonal contraception
Cervical ectropion, polyps or cancer
Sexually transmitted infection
Endometrial polyps or cancer
Vaginal pathology, including cancers
Pregnancy
Ovulation can cause spotting in some women
Medications, such as SSRIs and anticoagulants

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5
Q

Differentials for abnormal uterine bleeding?

A

Extremes of reproductive age (early periods or perimenopause)
Polycystic ovarian syndrome
Physiological stress (excessive exercise, low body weight, chronic disease and psychosocial factors)
Medications, particularly progesterone only contraception, antidepressants and antipsychotics
Hormonal imbalances, such as thyroid abnormalities, Cushing’s syndrome and high prolactin

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6
Q

Differentials for dysmenorrhoea?

A

Primary dysmenorrhoea (no underlying pathology)
Endometriosis or adenomyosis
Fibroids
Pelvic inflammatory disease
Copper coil
Cervical or ovarian cancer

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7
Q

Differentials for mennorhagia?

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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8
Q

Differentials for post coital bleeding?

A

Cervical cancer, ectropion or infection
Trauma
Atrophic vaginitis
Polyps
Endometrial cancer
Vaginal cancer

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9
Q

Differentials for pelvic pain?

A

Urinary tract infection
Dysmenorrhoea (painful periods)
Irritable bowel syndrome (IBS)
Ovarian cysts
Endometriosis
Pelvic inflammatory disease (infection)
Ectopic pregnancy
Appendicitis
Mittelschmerz (cyclical pain during ovulation)
Pelvic adhesions
Ovarian torsion
Inflammatory bowel disease (IBD)

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10
Q

Differentials for vaginal discharge?

A

Bacterial vaginosis
Candidiasis (thrush)
Chlamydia
Gonorrhoea
Trichomonas vaginalis
Foreign body
Cervical ectropion
Polyps
Malignancy
Pregnancy
Ovulation (cyclical)
Hormonal contraception

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11
Q

What is primary amenorrhoea?

A

Not starting menstruation

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12
Q

What are the types of hypogonadism?

A

Hypogonadotropic; lack of LH and FSH released from pituitary gland

Hypergonadotropic; lack of response to LH and FSH by the gonads

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13
Q

Causes of hypogonadotropic hypogonadism amenorrhoea?

A

Hypopituitarism
Damage to pituitary/ hypothalamus from radiotherapy, surgery
Cystic fibrosis
Excessive exercise/ dieting
Constitutional delay in development
Endocrine disorders; growth hormone deficiency, hypothyroidism, cushings, hyperprolactinaemia
Kallman syndrome

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14
Q

Causes of hypergonadotropic hypogonadism?

A

Previous damage to gonad; torsion, cancer, infection, mumps
Congenital absence
Turner syndrome
Androgen insensitivity
Congenital adrenal hyperplasia

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15
Q

What structural pathologies can present with amenorrhoea?

A

Imperforate hymen
Transverse vaginal septae
Vaginal agenesis
Absent uterus
FGM

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16
Q

Investigations to assess cause of amenorrhoea?

A

FBC; anaemia
U+E; CKD
Coeliac screen
Hormone panel; FSH, LH, TFT, IGF-1, Prolactin, Testosterone
Genetic testing
X-ray wrist
Pelvic USS
MRI of brain

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17
Q

Management of primary amenorrhoea?

A

Replacement hormones
Reduce stress
Gain/ lose weight
Pulsatile GnRH
COCP

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18
Q

What is secondary amenorrhoea?

A

Pregnancy
Menopause
Premature ovarian failure
Hormonal contraception
Hypothalamic pituitary pathology
Ovarain; PCOS
Uterine; ashermas syndrome
Thyoid pathology
Hyperprolactinaemia
Pituitary failure; trauma, radiotherapy, sheehan syndrome

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19
Q

What is premenstrual syndrome?

A

Psychological, physical and emotional symptoms that occur during the luteal phase of the menstrual cycle

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20
Q

Pathophysiology of premenstrual syndrome?

A

Fluctuation of oestrogen and progesterone during menstrual cycle

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21
Q

Presentation of premenstrual syndrome?

A

Low mood
Anxiety
Mood swings
Irritability
Bloating
Headache
Fatigue
Breast pain
Reduced confidence
Clumsiness
Reduced libido

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22
Q

How is premenstrual syndrome diagnosed?

A

Clinical diagnosis
Administration of GnRH analogues to see if symptoms resolve

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23
Q

Management of premenstrual syndrome?

A

General healthy lifestyle
COCP- containing drospirenone
SSRI antidepressant
CBT
GnRH analogues
Hysterectomy and bilateral oophorectomy
Danazole and tamoxifen for breast pain
Spironolactone

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24
Q

What defines menorrhagia?

A

> 80 mls blood loss

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25
Q

Causes of menorrhagia?

A

Idiopathic
Extreme of reproductive age
Endometriosis/ adenomyosis
Fibroids
Pelvic inflammatory disease
Contraceptives; especially copper coil
Anticoagulant medication
Bleeding disorder
Endocrine disorder
Connective tissue disorder
Endometrial hyperplasia/ cancer
PCOS

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26
Q

What to ask when taking a menstrual history?

A

Age at menarche
Cycle length, days menstruation and variation
Intermenstrual bleeding and post coital bleeding
Contraceptive history
Sexual history
Possibility of pregnancy
Plans for future pregnancy
Cervical.screening history
Migraines with/without aura
Past medical history and drug history
Smoking and alcohol history
Family history

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27
Q

Investigations to diagnose menorrhagia?

A

Speculum and bimanual pelvic examination; fibroids, ascites, cancer
FBC; IDA
Hysteroscopy; fibroids, endometrial pathology
Pelvic and transvaginal USS; large fibroids, adenomyosis, obesity, declined hysteroscopy
Coagulation screen
TFT

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28
Q

Management of menorrhagia?

A

Symptomatic relief; tranexamic acid, mefenamic acid

When contraception is allowed;
Mirena coil- first line
COCP
Cyclical oral progesterone

Endometrial ablation, Hysterectomy

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29
Q

What is a uterine fibroid?

A

Benign tumours of the smooth muscle of the uterus which are oestrogen sensitive
AKA Uterine leiomyoma

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30
Q

Types of uterine fibroids?

A

Intramural; within the myometrium
Subserosal; just below the outer layer and grow outward into the abdominal cavity
Submucosal; found below the endometrium
Pedunculated; on a stalk

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31
Q

Presentation of uterine fibroids?

A

Menorrhagia
Prolonged menstruation
Abdominal pain worse on menstruation
Bleeding/ feeling full in abdomen
Urinary/ bowel symptoms due to pelvic pressure
Deep dyspareunia
Reduced fertility

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32
Q

Investigations to assess uterine fibroids?

A

Abdominal/ bimanual examination; palpable pelvic mass
Hysteroscopy
Pelvic ultrasound
MRI Scan; before surgery to assess size, shape, blood supply

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33
Q

Management of fibroids?

A

Less than 3cm;
First line; mirena coil
NSAID, and tranexamic acid - symptom relief
Combined oral contraceptive
Cyclic oral progesterones
Surgery; endometrial ablation, resection, hysterectomy

More than 3cm;
Referal to gynaecology
Medical management same as above
Surgery; uterine artery embolisation, myomectomy, Hysterectomy

GnRH agonists maybe used preoperatively to reduce size of fibroids

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34
Q

Complications of uterine fibroids?

A

Iron deficiency anaemia
Reduced fertility
Pregnancy complications; miscarriages, premature labour, obstructive delivery
Constipation
Urinary outflow obstruction/ UTI
Red degeneration Of fibroid
Torsion of fibroid
Malignant change

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35
Q

What is red degeneration of fibroid?

A

Ischaemia, infarction and necrosis of the fibroid due to disrupted flow of blood supply and more likely to affect those larger than 5cm

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36
Q

Presentation of red degeneration of fibroid?

A

Severe abdominal pain
Low grade fever
Tachycardia
Vomiting

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37
Q

Risk factor for red degeneration of fibroid?

A

Pregnancy

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38
Q

Management of red degenration?

A

Fluids
Analgesia
Supportive

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39
Q

What is endometriosis?

A

Growth of ectopic endometrial tissue outside the uterine cavity

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40
Q

Aetiology of endometriosis?

A

Retrograde menstruation resulting in blood flow backwards into fallopian tube into peritoneum and pelvis

Endometrial cells destined to be uterine cells failed to migrate during embryonic development

Endometrial cells travel through lymphatics

Metaplasia of non endometrial cells

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41
Q

Presentation of endometriosis?

A

Cyclical abdominal/ pelvic pain
Deep dyspareunia
Dysmenorrhoea
Infertility
Cyclical bleeding from other sites

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42
Q

Investigations to diagnose endometriosis?

A

Pelvic ultrasound
Laparoscopy and biopsy - gold standard

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43
Q

Staging of endometriosis?

A

American society of reproductive medicine staging system;

Stage 1; small superficial lesions
Stage 2; mild, but deeper lesions compared to stage 1
Stage 3; deeper lesions, with lesions on ovaries and mild adhesions
Stage 4; deep and large lesions affecting ovaries with extensive adhesions

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44
Q

Management of endometriosis?

A

Initial management;
Establish diagnosis, educate patient and establish relationship
Analgesia

Hormonal management;
Combined pill
Progesterone only pill
Mirena coil
GnRH agonist

Surgical management;
Laparoscopic removal and ablation
Hysterectomy

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45
Q

What is adenomyosis?

A

Endometrial tissue within the myometrium

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46
Q

Risk factors for adenomyosis?

A

Later reproductive years
Multiparity
Hormone dependant

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47
Q

Presentation of adenomyosis?

A

Dysmenorrhoea
Menorrhagia
Dyspareunia

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48
Q

Investigations to diagnose adenomyosis?

A

First line- transvaginal USS
MRI or transabdominal ultrasound
Gold standard- histological

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49
Q

Management of adenomyosis?

A

Tranexamic acid, mefenamic acid

Mirena coil
COCP
Cyclical oral progestogens
GnRH analogues

Ablation
Uterine artery embolisation
Hysterectomy

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50
Q

Complications during pregnancy with adenomyosis?

A

Infertility
Miscarriage
Preterm birth
SGA
Preterm premature rupture of membrane
Malpresentation
Need for C-section
PPH

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51
Q

What is menopause?

A

Lack of menstruation for 12 months

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52
Q

What is the average age of menopause in UK?

A

51

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53
Q

What age is premature menopause diagnosed?

A

Before the age of 40 years

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54
Q

Hormonal changes that take place in menopause?

A

Oestrogen and progesterone are low
LH and FSH are high

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55
Q

Perimenopausal symptoms?

A

Hot flushes
Emotional lability
Premenstrual syndrome
Irregular menstruation
Joint pain
Heavier/ lighter periods
Vaginal dryness/ atrophy
Reduced libido

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56
Q

Risk associated with depleting oestrogen?

A

CVD and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

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57
Q

When should FSH blood test be considered in women presenting with perimenopausal symptoms?

A

Under 40 years with suspected premature menopause
40-45 years with symptoms and change in menstrual cycle

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58
Q

How long is contraception needed after last menstrual period?

A

2 years in women under 50 years
1 year in over 50 women

Since last menstrual period

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59
Q

UKMEC1 contraceptive options for women approaching menopause?

A

Barrier
Mirena/ copper coil
POP
Progesterone implant
Progesterone depot in under 45
Sterilisation

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60
Q

Why is progesterone depot not suitable for women over 45 years?

A

Reduced bone mineral density meaning higher risk of osteoporosis

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61
Q

Management of perimenopausal symptoms?

A

Nothing
HTR
Tibolone
Clonidine
CBT
SSRI antidepressant
Testosterone
Vaginal oestrogen/ moisturiser

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62
Q

What is premature ovarian insufficiency?

A

Menopause before the age of 40 years

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63
Q

Causes of premature ovarian insufficiency?

A

Idiopathic
Iatrogenic; chemotherapy, radiotherapy, surgery
Autoimmune
Genetics; turner’s syndrome
Infections; mumps, CMV, TB

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64
Q

When is premature insufficiency diagnosed?

A

Persistently raised FSH (>25) on two consecutive occassions 4 weeks apart in women under 40 years

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65
Q

Risks of premature ovarian insufficiency?

A

CVD
Stroke
Osteoporosis
Cognitive impairment
Dementia
Parkinsonism

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66
Q

Management of premature ovarian insufficiency?

A

HRT atleast until age of menopause either with traditional HRT or COCP

Manage VTE risk

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67
Q

What is HRT?

A

Treatment used in perimenopausal or postmenopausal women yo alleviate symptoms of menopause caused by the relative lack of oestrogen

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68
Q

Non hormonal treatment options for menopause?

A

Lifestyle changes; diet, exercise, weightloss, smoking cessation, reduce alcohol/ caffeine/ stress
CBT
Clonidine
SSRI antidepressants
Venlafaxine
Gabapentin

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69
Q

What is clonidine?

A

Alpha-2 adrenergic receptor agonist and imidazoline receptors in the the which lowers BP and reduced heart rate

Helps with vasomotor symptoms and hot flushes

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70
Q

Side effects of clonidine?

A

Dry mouth
Headache
Dizziness
Fatigue
Sudden withdrawal can result in rapid rise in BP and agitation

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71
Q

Alternative therapies for HRT?

A

Black cohosh- may cause liver damage
Dong quai; may cause bleeding disorder
Red clover; may have oestrogenic effects
Evening primrose; lots of interactions, seizures, clotting disorders

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72
Q

Indications for HRT?

A

Replacement of hormones in premature ovarian failure
Reduce vasomotor symptoms
Improve symptoms; low mood, low libido, poor sleep, joint pain
Reduce risk of osteoporosis in women under 60

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73
Q

Benefits of HRT?

A

Improved vasomotor symptoms; mood, urogenital, joint symptoms
Improved quality of life
Reduce risk of osteoporosis and fractures

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74
Q

Risk of HRT?

A

Increased risk of breast cancer, endometrial cancer
Increased VTE risk
Increased stroke and CVD

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75
Q

How can risks associated with HRT be reduced?

A

Endometrial cancer; progesterone
VTE; use patch rather than pill
Breast cancer, CVD; local progesterone rather than systemic

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76
Q

Contraindications to HRT?

A

Undiagnosed abnormal bleeding
Endometrial hyperplasia/ cancer
Breast cancer
Uncontrolled HTN
VTE
Liver disease
Active angina/ MI
Pregnancy

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77
Q

Assessment before commencing HRT?

A

Take history
Assess risk for oestrogen dependent cancer
Check BMI and blood pressure
Ensure cervical and breast cancer screening is upto date
Encourage lifestyle changes to minimise risks

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78
Q

How to chose formulation of HRT?

A

Local symptoms; topical oestrogen
Has uterus; combined HRT
No uterus; oestrogen only HRT
Perimenopausal; cyclical combined HRT
Post menopausal; continuous HRT

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79
Q

How long is a mirena coil licensed for endometrial protection?

A

4 yeas

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80
Q

Types of progestogens?

A

C19; testosterone derived- help to improve libido e.g norethisterone, levonorgestrel, desogestrel

C21; progesterone derived- help improve mood, acne e.g dydrogesterone, medroxyprogesterone

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81
Q

What is tibolone?

A

Synthetic steroid that stimulates oestrogen and progesterone receptors, weak androgen receptor stimulator

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82
Q

Cautions with tibolone?

A

Can cause irregular bleeding requiring further investigations to rule out other cause

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83
Q

Monitoring required for women on HRT?

A

Follow up in 3 months to monitor side effects when initiating
Problematic irregular bleeding should be refered to specialist
Stop oestrogen containing contraceptives 4 weeks before major surgery

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84
Q

Oestrogenic side effects of HRT?

A

Nausea and bloating
Breast swelling
Breast tenderness
Headaches
Leg cramps

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85
Q

Progestogenic side effects of HRT?

A

Mood swings
Bloating
Fluid retention
Weight gain
Acne and greasy skin

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86
Q

What is PCOS?

A

Metabolic and reproductive deranged characterised by androgen excess

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87
Q

What is the diagnostic criteria for PCOS?

A

Rotterdam criteria

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88
Q

Diagnostic criteria for PCOS?

A

2 of the following

Oligoovulation/ anovulation
Hyperandrogenism
Polycystic ovaries

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89
Q

Presentation of PCOS?

A

Oligomenorrhoea
Infertility
Obesity
Hirsutism
Acne
Hair loss in a male pattern
Ancanthosis nigricans

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90
Q

Complications of PCOS?

A

Insulin resistance and diabetes
Ancanthosis nigricans
CVD
Hypercholestrolaemia

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91
Q

Pathophysiology of insulin resistance in PCOS?

A

Insulin resistance results in increased pancreatic secretion of insulin
Insulin stimulates adrenal glands and ovaries to release androgens
Insulin suppresses sex hormone binding globulin production in liver which normally act to modulate androgen function

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92
Q

Investigations to diagnose PCOS?

A

LH, FSH; LH is raised more than FSH, increased LH to FSH ratio
Raised testosterone
Raised insulin

Pelvic ultrasound; string of pearls appearance

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93
Q

Diagnostic criteria for ultrasound scan appearance in PCOS?

A

12 or more developing follicles on one ovary
Ovarian volume >10 cm3

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94
Q

Gold standard investigation for PCOS?

A

Transvaginal ultrasound scan

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95
Q

Management of PCOS?

A

General lifestyle improvement to optimise risks associated with obesity, T2DM, CVD, hypercholesterolemia
Manage risk of endometrial cancer

Endometrial cancer risk reduction; mirena, cyclical progesterone, COCP

Fertility treatment; clomifene, laparoscopic ovarian drilling, IVF, metformin, letrozole

Manage hirsutism; Weightloss, Co-cyprindiol, topical eflornithine, electrolysis, laser, Spironolactone, Finasteride, flutamide,

Manage acne

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96
Q

Complications of PCOS?

A

Endometrial hyperplasia, cancer
Infertility
Hirsutism
Arne
Obstructive sleep apnoea
Depression/anxiety

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97
Q

Why are women with PCOS at higher risk of endometrial cancer?

A

Under normal circumstances corpus luteum produces progesterone, with infrequent ovulation there is unopposed oestrogen

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98
Q

Presentation of ovarian cysts?

A

Largely asymptomatic
Pelvic pain
Bloating
Fullness in abdomen
Palpable pelvic mass

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99
Q

Types of ovarian cysts?

A

Follicular cyst; developing follicle, most common type of cyst with thin walls and tend to disappear after a few cycles

Corpus luteum cysts; develops when corpus luteum fails to break down causing pelvic discomfort and delayed menstruation

Serous cystadenoma; tumours of the epithelial cells in the ovary

Mucinous cystadeoma; tumours of epithelial cells in patients with endometriosis causing pain and disrupt ovulation

Dermoid/ Germ cell tumours; benign ovarian teratoma arising from germ cells

Sex chord tumours; arise from stroma or sex chords and encompass several types of tumours

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100
Q

Investigations to assess ovarian cysts?

A

Premenopausal women with simple ovarian cysts less than 5cm on USS require no further tests

CA125 tumour marker

Women under 40 with complex ovarian mass require germ cell tumour markers;
Lactate dehydrogenase
Alpha fetoprotein
hCG

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101
Q

Causes of raised CA125?

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

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102
Q

What is risk of malignancy index and what does it take into account?

A

Estimates risk of ovarian mass being malignant

Menopausal status
Ultrasound finding
CA125

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103
Q

Management of ovarian cysts?

A

Possible ovarian cancer (Complex cyst or raised CA125) requires 2 week wait referral

Possible dermoid cyst requires referral for surgical removal

Simple ovarian cysts in pre-menopausal women management depends on size;
<5cm; does not require follow up scan and typically resolves in 3 cycles
5-7cm; routine referral to gynae and annual USS monitoring
>7cm; consider MRI for surgical removal

Simple cysts in postmenopaual women;
<5cm; review in 4-6 months
>5cm with raised CA125 requires 2 week wait referral to gynae

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104
Q

Complications of ovarian cyst?

A

Torsion
Haemorrhage
Rupture

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105
Q

Triad of Meig’s syndrome?

A

Ovarian fibroma
Pleural effusion
Ascites

Older women

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106
Q

Management of Meig’s syndrome?

A

Removal of tumour results in resolution of symptoms

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107
Q

What is ovarian torsion?

A

Twisting of the ovary in relation to surrounding connective tissue, fallopian tube and blood supply

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108
Q

Causes of ovarian torsion?

A

Large cysts
Long indofundibular ligament

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109
Q

Presentation of ovarian torsion?

A

Sudden onset severe unilateral pelvic pain
Localised tenderness
Palpable mass

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110
Q

Management of ovarian torsion?

A

Laparoscopic surgery;
Detorsion
Oophorectomy

Decision is made during surgery

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111
Q

How is ovarian torsion diagnosed?

A

Pelvic USS; whirlpool sign, free fluid and oedematous ovary

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112
Q

Complications of ovarian torsion?

A

Delay in treatment can result in loss of ovary
Infection
Abscess, sepsis
Rupture
Intra-abdominal adhesions
Peritonitis

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113
Q

What is asherman’s syndrome?

A

Intrauterine adhesions as a result of uterine damage

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114
Q

Causes of ashermans syndrome?

A

D+C procedure
Following uterine surgery
Pelvic infection

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115
Q

Presentation of ashermans syndrome?

A

Secondary amenorrhoea
Lighter periods
Dysmenorrhoea
Infertility

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116
Q

Investigations to diagnose ashermans syndrome?

A

Hysteroscopy
Hysterosalpingogram
MRI scan

Usually found incidently

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117
Q

Gold standard investigation for ashermans syndrome?

A

Hysteroscopy due to option of treating

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118
Q

What is cervical ectropion?

A

Columnar epithelium of endocervix extends out to the ectocervix, these columnar epithelial cells are more fragile and prone to bleeding and is associated with elevated oestrogen

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119
Q

What is the transformation zone?

A

Border between columnar epithelium of the endocervix and the stratified squamous epithelium of the ectocervix

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120
Q

Presentation of cervical ectropian?

A

Asymptomatic and found on speculum examination
Increased vaginal discharge, bleeding
Dyspareunia
Post coital bleeding

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121
Q

Management of cervical ectropion?

A

If asymptomatic do nothing

Cauterisation of the ectropion using silver nitrate or cold coagulation

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122
Q

What is a nabothian cyst?

A

Fluid filled cyst seen on the surface of the cervix upto 1cm in size and harmless

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123
Q

Presentation of nabothian cyst?

A

Often found incidentally on speculum examination
Smooth rounded bumps on the cervix near the os with a white/ yellow appearance

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124
Q

Management of nabothian cyst?

A

Nothing

If suspicious of cancer, biopsy

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125
Q

What is pelvic organ prolapse?

A

Descent of pelvic organs into vagina due to weakness of ligaments and muscles surrounding uterus, rectum and bladder

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126
Q

Types of pelvic organ prolapse?

A

Uterine prolapse; uterus descends into vagina
Vault prolapse; when women have had hysterectomy the vault of the uterus (the top) descends into the vagina
Rectocele; defects in posterior vaginal wall allow rectum to prolapse forward into vagina
Cystocele; defect in anterior vaginal wall allowing bladder to prolapse backward into vagina

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127
Q

Risk factors for pelvic organ prolapse?

A

Multiple vaginal deliveries
Instrumental, prolonged, traumatic delivery
Advanced age
Post menopause
Obesity
Chronic respiratory disease causing coughing
Chronic constipation and straining

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128
Q

Presentation of pelvic organ prolapse?

A

Feeling something coming down into vagina
Dragging or heavy sensation in pelvis
Urinary symptoms
Bowel symptoms
Sexual dysfunction
May feel lump or mass in vagina

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129
Q

Investigations to assess pelvic organ prolapse?

A

Sim’s speculum

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130
Q

Grades of uterine prolapse?

A

Pelvic organ prolapse quantification (POP-Q);
Grade 0; Normal
Grade 1; lowest part is more than 1cm above introitus
Grade 2; lowest part is within 1cm of the introitus
Grade 3; lowest part is more than 1cm below the introitus but not fully descended
Grade 4; full descent with inversion of the uterus

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131
Q

What is uterine procidentia?

A

Prolapse extending beyond introitus

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132
Q

Management of pelvic organ prolapse?

A

Conservative;
Physiotherapy, weight loss, lifestyle change, treatment of related symptoms, vaginal oestrogen cream

Vaginal pessary;
Ring shape, Shelf and gellhorn, Cube, Donut, Hodge

Surgery;
Definitive treatment

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133
Q

Complications of pelvic organ prolapse surgery?

A

Pain, bleeding, infection, DVT, risk of anaesthetic
Damage to bladder/ bowel
Recurrence of prolapse
Altered sexual function

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134
Q

Complications of mesh repair of pelvic organ prolapse?

A

Chronic pain
Altered sensation
Dyspareunia
Abnormal bleeding
Urinary/ bowel symptoms

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135
Q

Types of incontinence?

A

Urge; detrusor muscle overactivity which means patient has sudden urge to urinate

Stress; pelvic floor weakness and sphincter weakness

Mixed; mixture of stress and urge incontinence

Overflow; chronic urinary retention

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136
Q

Risk factors for urinary incontinence?

A

Parity
Vaginal delivery
Increasing age
Post menopausal
High BMI
Pelvic organ prolapse
Pelvic floor surgery
Neurological conditions
Cognitive impairement

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137
Q

Lifestyle factors that contribute to urinary incontinence?

A

Caffeine consumption
Alcohol
Medications
BMI

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138
Q

Modified oxford grading system for pelvic muscle strength?

A

Grade 0; no contraction
Grade 1; faint contraction
Grade 2; weak contraction
Grade 3; moderate contraction with some contraction
Grade 4; good contraction with resistance
Grade 5; strong contraction, a firm squeeze and drawing inwards of examining fingers

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139
Q

Investigations performed to diagnose urinary incontinence?

A

Bladder diary
Urine dipstick
Post void residual bladder volume
Urodynamic testing

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140
Q

Management of stress incontinence?

A

Lifestyle management
Supervised pelvic floor exercises; for atleast 3 months
Surgery
Duloxetine

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141
Q

Management of urge incontinence?

A

Bladder retraining
Anticholinergic medication; oxybutynin, tolterodine, solifenacin
Mirabegron
Invasive procedure; botox injection, percutaneous sacral nerve stimulation, augmentation cystoplasty, urinary diversion

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142
Q

What is a contraindication to mirabegron?

A

Hypertension as it is a beta-3 agonist

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143
Q

What is atrophic vaginitis?

A

Dryness and atrophy of the vaginal mucosa due to a lack of oestrogen

144
Q

Pathophysiology of atrophic vaginitis?

A

Lack of oestrogen results in thinner vaginal mucosa which is less elastic and dry and more prone to inflammation

145
Q

Presentation of atrophic vaginitis?

A

Itching
Dryness
Dyspareunia
Bleeding due to localised inflammation

Recurrent UTI, stress incontinence, pelvic organ prolapse

146
Q

Examination findings in atrophic vaginitis?

A

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

147
Q

Management of atrophic vaginitis?

A

Oestrogen cream, pessary, ring or tablets

148
Q

Contraindications to topical oestrogen?

A

Breast cancer
Angina
VTE

149
Q

What is bartholin’s cyst?

A

Blockage in ducts for bartholin’s gland becomes blocked resulting in swelling, erythema

150
Q

Management of bartholins cyst?

A

Analgesia, cleanliness
Abscess requires antibiotics
Severe cases may require surgical removal

151
Q

What is lichen sclerosus?

A

Chronic inflammatory skin condition presenting as patches of shiny, porcelain white skin commonly affecting labia, perineum, perianal skin

152
Q

Presentation of lichen sclerosus ?

A

Itching
Soreness and pain, possibly worse at night
Skin tightness
Superficial pyspareunia
Erosions
Fissures
Koebners phenomenon

Skin changes; porcelain white, shiny, tight, thin, slightly raised, papules or plaques

153
Q

Management of lichen sclerosus?

A

Follow-up every 3-6 months
Clobetasol propionate
Emollients

154
Q

Complications of lichen sclerosus?

A

5% risk of squamous cell carcinoma of the vulva
Pain and discomfort
Sexual dysfunction
Bleeding
Narrowing of vaginal/ urethral openings

155
Q

What is FGM?

A

Surgically changing female genitalia for non medical reasons and is illegal under the Female Genital Mutilation act of 2003

156
Q

Epidemiology of FGM?

A

Common cultural practice in parts of africa
Somalia has the highest rate
Other countires, ethopia, sudan, yemen, indonesia

157
Q

Types of FGM?

A

Type 1; removal of part or all of clitoris
Type 2; removal of part or all of the clitoris and labia minora
Type 3; narrowing and closure of the vaginal orifice
Type 4; all other unnecessary procedures

158
Q

Complications of FGM?

A

Immediate;
Pain, bleeding, infection, swelling, urinary retention, urethral damage and incontinence

Long term complications;
Vaginal infections, pelvic infection, UTI, dysmenorrhoea, sexual dysfunction, infertility and pregnancy related complications, psychological issues, reduced engagement with screening and healthcare

159
Q

Management of FGM?

A

Report all cases under 18 to the police
Social services, paediatrics, FGM services, counselling

160
Q

What is a bicornate uterus?

A

Two horns to the uterus and is associated with poor obstetric outcomes such as miscarriage, PTB, malpresentation

161
Q

What is an imperforate hymen?

A

Hymen at entrance of vaginal orifice is completely sealed presenting with cyclical abdominal pain with no vaginal bleeding and needs an incision to treat

Can lead to retrograde menstruation and hence endometriosis

162
Q

What are transverse vaginal septae?

A

Septum which sit transversely across vagina which can be perforate or imperforate

Problems with tampon use and sexual intercourse

If imperforate can present similar to imperforate hymen

163
Q

What is vaginal hypoplasia/ agenesis?

A

Abnormally small vagina/ absent vagina due to errors in mullarian duct development

Treated with vaginal dilator

164
Q

Inheritance pattern of androgen insensitivity syndrome?

A

X-linked recessive

165
Q

What is androgen insensitivity syndrome?

A

Cells are not able to respond to androgens due to lack of androgen receptors in genetically male patients with female secondary sexual characteristics

166
Q

Presentation of androgen insensitivity syndrome?

A

Inguinal hernia in infancy or primary amenorrhoea in puberty

Biological male with female secondary charatceristics

No uterus, upper vagina, fallopian tubes and ovaries as testes produce AMH

Lack of androgen conversion to testosterone, high oestrogen

167
Q

Most common type of cervical cancer?

A

Squamous cell carcinoma of the cervix accounts for upto 80% of cases

Adenocarcinoma is the next most common

168
Q

What HPV strains are linked to cervical cancer?

A

16 and 18

169
Q

How to HPV strains contribute to cancer?

A

Produces proteins E6 and E7 which are responsible for inhibiting tumour suppressor genes promoting development of cancer

E6 inhibits p53
E7 inhibits pRb

170
Q

Risk factors for cervical cancer?

A

Increased risk of HPV
Non engagement with screening
Smoking
HIV
COCP
Increased number of full term pregnancies
Family history
Exposure to diethylstilbestrol

171
Q

Presentation of cervical cancer?

A

Asymptomatic- picked up on screening
Intermenstrual/ post coital/ post menopausal bleeding
Pelvic pain
Dyspareunia

172
Q

Appearance on colposcopy suggestive of cancer?

A

Ulceration
Inflammation
Bleeding
Visible tumour

173
Q

What is the Cervical Intraepithelial Neoplasia grading system?

A

CIN 1; mild dysplasia, affecting 1/3 the thickness of the epithelial layer and is likely to return to normal without treatment

CIN 2; moderate dysplasia affecting 3/3 thickness, likely to progress to cancer if untreated

CIN 3; severe dysplasia, very likely to progress to cancer if untreated (AKA cervical carcinoma insitu)

174
Q

What is the age for cervical screening and frequency?

A

Every 3 years aged 25-49
Every 5 years aged 50-64

HIV positive screened annually
Women with previous CIN require additional tests
Immunocompromised women may have additional tests
Pregnant women due routine smear should wait 12 weeks post partum

175
Q

Actions to take after smear result?

A

Inadequate sample; repeat smear after 3 months
HPV negative; return to routine screening
HPV positive with normal cytology; repeat HPV test in 12 months
HPV positive and abnormal cytology; refer to colposcopy

176
Q

What type of sample is taken during cervical screening?

A

Liquid based cytology

177
Q

What tests are performed during colposcopy?

A

Acetic acid; abnormal cells appear white

Schiller’s iodine test; healthy cells stain brown, unhealthy cells do not stain

Punch biopsy or large loop excision of transformational zone can be performed

178
Q

Risk associated with loop biopsy?

A

Preterm birth

179
Q

What is a cone biopsy

A

Treatment for CIN where a cone shaped piece of the cervix is removed

180
Q

Risks of cone biopsy?

A

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

181
Q

Staging of cervical cancer?

A

Stage 1; confined to cervix
Stage 2; invades uterus or upper 2/3 of vagina
Stage 3; Invades pelvic wall or lower 1/3 of vagina
Stage 4; Involves bladder, rectum or beyond pelvis

182
Q

Management of cervical cancer?

A

CIN and early stage 1A; LLETZ, Cone biopsy

Stage 1B- 2A; radical hysterectomy and removal of local lymph nodes +/- chemotherapy, radiotherapy

Stage 2B- 4A; chemotherapy, radiotherapy

Stage 4B; combination therapy and palliative care

Pelvic exenteration; removal of most of the pelvic organs

183
Q

What type of endometrial cancer is most common?

A

Adenocarcinoma

184
Q

What is endometrial hyperplasia?

A

Pre-cancerous condition with thickened endometrium, only 5% go on to develop cancer

185
Q

Treatment of endometrial hyperplasia?

A

Progesterone

186
Q

Is endometrial cancer oestrogen dependant?

A

Yes

Risk factors include those that increase oestrogen exposure

187
Q

Risk factors for endometrial cancer?

A

Increased age
Earlier onset menstruation
Late menopause
Oestrogen only HRT
No or few pregnancies
Obesity
PCOS
Tamoxifen- anti-oestrogen on breast tissue but pro-oestrogen on endometrium
T2DM

188
Q

Protective factors for endometrial cancer?

A

COCP
Mirena coil
Increased pregnancies
Cigarette smoking

189
Q

Presentation of endometrial cancer?

A

Postcoital bleeding
Intermenstrual bleeding
Menorrhagia
Abnormal vaginal discharge
post menopausal bleeding
Haematuria
Anaemia
Raised platelet count

190
Q

Indications to transvaginal USS in suspected endometrial cancer?

A

Over 55 years with
Unexplained vaginal discharge
Visible haematuria
And one of; raised platelets, anaemia, elevated glucose

191
Q

Investigations to diagnose endometrial cancer?

A

Transvaginal USS for endometrial thickness
Pipelle biopsy
Hysteroscopy with endometrial biopsy

192
Q

What is normal endometrial thickness in post-menopausal women?

A

<4mm

193
Q

Staging for endometrial cancer?

A

Stage 1; confined to uterus
Stage 2; invades into cervix
Stage 3; invades ovaries, fallopian tubes, vagina, lymph nodes
Stage 4; invades bladder, rectum, beyond pelvis

194
Q

Management of endometrial cancer?

A

Stage 1 and 2; total abdominal hysterectomy with bilateral salpingo-oophorectomy

Other options;
Radical hysterectomy
Radiotherapy
Chemotherapy
Progesterone

195
Q

When does ovarian cancer present?

A

late stages, 70% present when it has spread to other organs

196
Q

Types of ovarian cancers?

A

Epithelial cell cancers;
Serous
Endometrioid carcinomas
Clear cell tumour
Mucinous tumour
Undifferentiated tumour

Dermoid cyst/ germ cell tumour
Sex chord/ stromal tumour
Metastasis

197
Q

What is a krukenberg tumour?

A

Metastasis to the ovary

198
Q

Risk factors for ovarian cancer?

A

Age; peak at 60
BRCA1 and BRCA2
Increased number of ovulations
Obesity
Smoking
Recurrent use of clomifene

199
Q

Presentation of ovarian cancer?

A

Abdominal bloating
Early satiety
Loss of appetite
Pelvic
Urinary symptoms
Weight loss
Abdominal or pelvic mass
Ascites

Hip/ groin pain- obturator nerve

199
Q

When is a CA125 blood test indicated for suspected ovarian cancer?

A

Woman over 50 years old with;
New symptoms of IBS
Abdominal bloating
Early satiety
Pelvic pain
Urinary frequency/ urgency
Weight loss

199
Q

Investigations to diagnose ovarian cancer?

A

CA125 blood test (>35 is significant)
Pelvic ultrasound
CT scan
Histology
Paracentesis

199
Q

Referral criteria under 2 week wait for suspected ovarian cancer?

A

Ascites
Pelvic mass
Abdominal mass

199
Q

Staging system for ovarian cancer?

A

Stage 1; confined to ovary
Stage 2; spread past ovary but confined to pelvis
Stage 3; spread past pelvis but in abdomen
Stage 4; spread outside abdomen

200
Q

What is risk of malignancy index?

A

Estimates risk of ovarian mass being malignant accounting for menopausal status, USS findings, CA125 level

200
Q

Management of ovarian cancer?

A

Combination of surgery and chemotherapy

200
Q

Most common type of vulval cancer?

A

Squamous cell carcinoma

200
Q

Types of vulval intraepithelial neoplasia?

A

High grade squamous intraepithelial neoplasia; HPV infection typically occurs in 35-50 years

Differentiated VIN; associated with lichen sclerosis in women 50-60

200
Q

Risk factors for vulval cancer?

A

Advanced age
Immunosuppression
HPV infection
Lichen sclerosus - 5% of patients develop vulval cancer

200
Q

Management of VIN?

A

Watch and wait
Wide local excision
Imiquimod cream
Laser ablation

201
Q

Presentation of vulval cancer?

A

Vulval lump
ulceration
Bleeding
Pain
Itching
Lymphadenopathy

202
Q

What is bacterial vaginosis?

A

Overgrowth of anaerobic bacteria in the vagina due to depletion of lactobacili in the vagina

203
Q

What are lactobacili?

A

Main component of vaginal flora that produce lactic acid to maintain vaginal pH

204
Q

Bacteria associated with bacterial vaginosis?

A

Gardnerella vaginalis
Mycoplasma hominis
Prevotella species

205
Q

Risk factors for bacterial vaginosis?

A

Multiple sexual partners
Excessive vaginal cleaning
Recent antibiotics
Smoking
Copper coil

206
Q

Presentation of bacterial vaginosis?

A

Fishy smelling vaginal discharge

207
Q

Investigations to diagnose bacterial vaginosis?

A

Clinical diagnosis with speculum examination
High vaginal swab to rule out STD and speculum examination
Vaginal pH
Microscopy reveals clue cells

208
Q

What are clue cells?

A

Cervical epithelial cells that contain gardnerella vaginalis

209
Q

Management of bacterial vaginosis?

A

Nothing resolves on its own

Can give Metronidazole, second line is clindamycin

210
Q

Complications of bacterial vaginosis?

A

Increased risk of developing STI

Pregnancy associated;
Miscarriage, preterm delivery, premature rupture of membranes, chorioamnionitis, low birth weight, post partum endometritis

211
Q

What is candidasis?

A

Vaginal infection with yeast of the Candida family

Most commonly candida albicans

212
Q

Risk factors for candidasis?

A

Pregnancy
Poorly controlled diabetes
Immunosuppression
Broad spectrum antibiotics

213
Q

Investigations to diagnose candidasis?

A

Vaginal pH
Charcoal swab for microscopy

214
Q

Management of candidasis?

A

Antifungal cream (clotrimazole)
Antifungal pessary (clotrimazole)
Antifungal tablets (fluconazole)

Treatment regime options
Single dose of intravaginal clotrimazole cream at night
Single dose of 500mg clotrimazole pessary at night
Three doses of clotrimazole 200mg pessary over 3 nights
Single dose of oral fluconazole 150mg

215
Q

Advice to women taking Antifungal creams and pessarys?

A

Damage condoms and reduce effectiveness of spermicide so consider other forms of contraception

216
Q

Most common STI in UK?

A

Chlamydia

217
Q

What type of organism is chlamydia?

A

Gram negative intracellular organism

218
Q

What STIs are screened for when attending GUM clinic?

A

Chlamydia
Gonorrhoea
Syphilis
HIV

219
Q

What is a charcoal swab?

A

Used in GUM clinics for microscopy, culture and sensitivities

Can identify; bacterial vaginosis, gonorrhoea, candidiasis, trichomonas vaginalis, other bacteria

220
Q

What is a NAAT test?

A

Checks DNA/ RNA of microorganism specifically chlamydia and gonorrhoea

vulvovaginal, endocervical swab
First catch urine
Urethral swab
Rectal, pharyngeal swab

221
Q

Presentation of chlamydia?

A

Asymptomatic
Abnormal vaginal discharge
Pelvic pain
Abnormal vaginal bleeding
Dyspareunia
Dysuria

Men;
Urethral discharge
Dysuria
Epididymo-orchitis
Reactive arthritis

222
Q

How is chlamydia diagnosed?

A

NAAT test

223
Q

Management of chlamydia?

A

First line for uncomplicated infection; doxycycline 100mg BD for 7 days

Alternative for pregnant or breastfeeding women;
Azithromycin 500mg QDS for 2 days
Erythromycin 500mg QDS for 7 days or BD for 14 days
Amoxicillin 500mg TDS

224
Q

When is doxycycline contraindicated?

A

Pregnant or breastfeeding women

225
Q

Other advice given to patients diagnosed with chlamydia?

A

Abstain from sex for 7 days
Refer all close contacts for contact tracing
Test for treat any other STIs
Advice to prevent future infection
Consider safeguarding

226
Q

Complications of chlamydia infection?

A

Pelvic inflammatory disease
Chronic pelvic pain
Infertility
Ectopic pregnancy
Epididymo-orchitis
Conjunctivitis
Lymphogranuloma venereum
Reactive arthritis

Pregnancy related complications;
Preterm delivery
Premature rupture of membranes
Low birth weight
Post partum endometritis
Neonatal infection

227
Q

What is lymphogranuloma venereum?

A

Condition affecting lymphoid tissue around site of infection more commonly in men who have sex with men

228
Q

Stages of lymphogranuloma venereum?

A

Primary stage; painless ulcer usually on penis, vaginal wall, rectum

Secondary stage; lymphadenitis, swelling, inflammation and pain in lymph nodes

Tertiary stage; inflammation of the rectum

229
Q

Management of lymphogranuloma venereum?

A

Doxycycline 100mg BD for 21 days

Alternatives erythromycin, azithromycin, ofloxacin

230
Q

What does gonorrhoea infect?

A

Mucous membranes with columnar epithelium such as endocervix, urethra, rectum, conjunctiva and pharynx

231
Q

Type of microorganism is gonorrhoea?

A

Gram negative diplococcus

232
Q

Presentation of gonorrhoea?

A

Odourless purulent discharge, maybe green or yellow in colour
Dysuria
Pelvic pain

Testicular pain or swelling

Pharyngeal infection

Rectal pain

Conjunctivitis

233
Q

How is gonorrhoea diagnosed?

A

NAAT
Charcoal swab

234
Q

Management of gonorrhoea?

A

Single dose of IM ceftriaxone 1g if sensitivities are not known
Single dose of oral ciprofloxacin 500mg if sensitivities are known

235
Q

What is a test of cure?

A

Follow up test after receiving treatment for gonorrhoea with NAAT testing

72 hours after treatment for culture
7 days after for RNA NAAT
14 days after for DNA NAAT

236
Q

Complications of gonorrhoea?

A

Pelvic inflammatory disease
Chronic pelvic pain
Infertility
Epididymo- orchitis
Prostatitis
Conjunctivitis
Urethral strictures
Disseminated gonococcal infection
Skin lesions
Fitz- Hugh- Curtis syndrome
Endocarditis

236
Q

What is ophthalmia neonatorum?

A

Gonococcal conjunctivitis of neonate due to maternal infection during pregnancy

237
Q

Complications of ophthalmia neonatorum?

A

Sepsis
Perforation of eye
Blindness

238
Q

What is disseminated gonococcal infection?

A

Complication of untreated gonorrhoea where bacteria spreads to skin and joints causing;
Various non specific skin lesions
Polyarthralgia
Migratory polyarthritis
Tenosynovitis
Systemic symptoms

239
Q

What is mycoplasma genitalium?

A

Bacteria causing non gonococcal urethritis

240
Q

What is the purpose of test of cure?

A

High level of antibiotic resistance

241
Q

Complications of mycoplasma genitlium?

A

Epididymitis
Cervicitis
Endometritis
Pelvic inflammatory disease
Reactive arthritis
Preterm delivery in pregnancy
Tubal infertility

242
Q

Key feature of mycoplasma genitalium?

A

Urethritis

243
Q

Investigations to diagnose mycoplasma genitalium?

A

NAAT; first urine sample in men, vaginal swabs in women

244
Q

Management of mycoplasma genitalium?

A

Doxycycline 100mg BD for 7 days then azithromycin 1g stat then 500mg OD for 2 days

Azithromycin alone in pregnancy and breastfeeding

245
Q

What is pelvic inflammatory disease?

A

Inflammation and infection of pelvic organs caused by infection spreading up through cervix

246
Q

Causes of PID?

A

STI; neisseria gonorrhoea, chlamydia, mycoplasma genitalium

Haemophilus influnezae, e.coli

247
Q

Risk factors for PID?

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing STI
Previous PID
IUD

248
Q

Presentation of PID?

A

Pelvic/ lower abdominal pain
Abnormal vaginal discharge
Abnormal vaginal bleeding
Dyspareunia
Fever
Dysuria

249
Q

Pelvic examination findings in PID?

A

Pelvic tenderness
Cervical motion tenderness
Inflammed cervix
Purulent discharge

250
Q

Investigations to diagnose PID?

A

NAAT swabs
HIV test
Syphilis test
High vaginal swab for bacterial vaginosis, candidiasis, trichomoniasis
Inflammatory markers

251
Q

Management of PID?

A

Referral to GUM
Single dose of 1g IM ceftriaxone to cover gonorrhoea
Doxycycline 100mg BD for 14 days covers chlamydia and mycoplasma genitalium
Metronidazole 400mg BD for 14 days

252
Q

Complications of PID?

A

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

253
Q

What is Fitz-Hugh-Curtis syndrome?

A

Complication of PID caused by inflammation and infection of the liver capsule leading to adhesions between liver and peritoneum presenting as RUQ pain and reffered right shoulder tip pain

254
Q

What is trichomoniasis?

A

Infection of protozoan parasite called trichomonas vaginalis, a single celled organism

255
Q

Complications of trichomoniasis infection?

A

Increased risk of contracting HIV
Bacterial vaginosis
Cervical cancer
PID
Pregnancy related complications

256
Q

Presentation of trichomoniasis infection?

A

Vaginal discharge; frothy, yellow green fishy smell
Itching
Dysuria
Dyspareunia
Balanitis

Strawberry cervix on examination

Raised vaginal pH

257
Q

Diagnosis of trichomoniasis infection??

A

Charcoal swab for microscopy
Swab from posterior fornix of vagina
Urethral swab
First catch urine

258
Q

Management of trichomoniasis infection?

A

GUM contact tracing
Metronidazole

259
Q

Features of chlamydial conjunctivitis?

A

Chronic erythema
Irritation
Discharge for more than 2 weeks

260
Q

What is gonorrhoea?

A

Infection with gram negative diplococcus affecting mucous membranes with columnar epithelium such as endocervix, urethra, rectum, conjunctiva and pharynx

261
Q

Is test of cure indicated for chlamydia?

A

No

262
Q

Is routine test of cure indicated for gonorrhoea?

A

Yes

263
Q

Investigations to diagnose mycoplasma genitalium?

A

First urine sample, vaginal swab NAAT

264
Q

Risk factors for PID and STIs?

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing STI
Previous PID
IUD

265
Q

Investigations to diagnose trichomonas vaginalis?

A

Charcoal swab

265
Q

Where does HSV lie in the latent phase?

A

Associated sensory nerve ganglia

Trigeminal nerve ganglion for cold sores (HSV1)

Sacral nerve ganglion for genital herpes (HSV2)

266
Q

Presentation of genital herpes?

A

Ulcers/ blistering ulcers
Neuropathic pain; tingling, shooting, burning
Flu like symptoms
Dysuria
Inguinal lymphadenopathy

267
Q

Investigations to diagnose genital herpes?

A

Viral PCR

268
Q

Management of genital herpes?

A

GUM referral
Lidocaine
Aciclovir

269
Q

Complications of herpes in pregnancy?

A

Not known to cause any complications but can be passed to foetus during birth

270
Q

How is genital herpes treated in pregnancy?

A

Before 28 weeks treated with aciclovir during infection and prophylactic treatment from 36 weeks until delivery, vaginal birth if asymptomatic

After 28 weeks; aciclovir for infection followed by regular prophylaxis and C-section delivery

271
Q

Complication of neonatal herpes simplex infection?

A

High rate of mortality and morbidity

272
Q

Type of virus is HIV?

A

RNA retrovirus

273
Q

Examples of AIDS defining illness?

A

Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia
CMV infection
Candidasis
Lymphoma
Tuberculosis

274
Q

Testing for HIV?

A

Antibody test
p24 antigen
PCR; number of viral copies and hence viral load

275
Q

How is HIV monitored?

A

CD4 count;
500-1200 cells/ mm3 is normal
Below 200 is end stage HIV

Viral load;
Undetectable is 50-100 copies/ ml

276
Q

Management of HIV?

A

HAART;
Protease inhibitors, integrase inhibitor, nucleoside reverse transcriptase inhibitors, nonnucleoside reverse transcriptase inhibitors, entry inhibitors

Prophylactic co-trimoxazole to protect against PCP

Monitor CVD risk

Vaccines upto date, avoid live vaccine

277
Q

Prophylactic treatment in neonate born to HIV mothers?

A

Zidovudine <50/ ml for 4 weeks

Zidovudine, lamivudine, nevirapine >50/ ml for 4 weeks

278
Q

Should HIV mothers breastfeed?

A

No, even if undetectable

279
Q

Causative agent for syphilis?

A

Treponema pallidum , spirochete

280
Q

Stages of syphilis?

A

Primary syphilis; painless ulcer (chancre)

Secondary syphilis; systemic symptoms which resolve in 3 to 12 weeks

Latent; asymptomatic but still infected

Tertiary; involes multiple organs, CVS and neurological complications

Neurosyphilis; infection involving CNS

281
Q

What is PEP?

A

Reduce risk of HIV transmission commenced within 72 hours of possible contact

282
Q

PEP regime?

A

Combination ART; Truvada (emttricitabine and tenofovir) and raltegravir for 28 days

Immediate HIV test and follow up in 3 months

283
Q

Presentation of syphilis?

A

Primary; chancre, local lymphadenopathy

Secondary; maculopapular rash, condylomata lata, low grade fever, lymphadenopathy, alopecia, oral lesion

Tertiary; gummas, aortic aneurysm, neurosyphilis

284
Q

Features of neurosyphilis?

A

Headache
Altered behaviour
Dementia
Tabes dorsalis
Ocular syphilis
Paralysis
Sensory impairment
Argyll Robertson pupil

285
Q

Investigations to diagnose syphilis?

A

T.pallidum antibody test
Dark field microscopy
PCR

286
Q

Concepts for contraception in older women?

A

After LMP contraception for 2 years under 50 and 1 year in over 50 years
Stop progesterone injection before 50

287
Q

Why does progesterone injection need to be stopped before 50?

A

Risk of osteoporosis

288
Q

When should progesterone only contraception be stopped?

A

FSH above 30 on two separate occasions 6 weeks apart

Age over 55

289
Q

Guidance around contraception under 20?

A

COCP, POP pill
IDU, coil have higher risk of expulsion

290
Q

Effectiveness of COCP?

A

99% with perfect use, typical use 91%

291
Q

COCP mechanism of action?

A

Prevents ovulation
Progesterone thickens cervical mucus and inhibits proliferation of endometrium

292
Q

Types of COCP?

A

Monophasic
Multiphasic

293
Q

First line COCP?

A

Pill containing levonoregestrel or norethisterone

Pills containing drospirenone is first line for PMS

294
Q

Side effects of COCP?

A

Breast pain and tenderness
Unscheduled bleeding
Mood changes and depression
Headache
Hypertension
VTE
Increased risk of breast and cervical cancer
Increased risk of MI and stroke

295
Q

Benefits of COCP?

A

Effective contraception
Rapid return of fertility
Improvement in PMS, menorrhagia, dysmenorrhoea
Reduced risk of ovarian, endometrial and colon cancer
Reduced risk of benign ovarian cysts

296
Q

Contraindications for starting COCP?

A

Uncontrolled HTN
Migraine with aura
History of VTE
Age over 35 and smoking more than 15 per day
Major surgery with prolonged immobility
Vascular disease/ stroke
Ischaemic heart disease, cardiomyopathy, atrial fibrillation
Liver cirrhosis/ tumours
SLE/ antiphospholipid tumour

297
Q

When should COCP be commenced?

A

Day 1 of cycle

If after day 5 requires additional contraception for 7 days

If switching from POP requires additional contraception for 7 days

298
Q

Things to check before commencing COCP?

A

Age
Height, BMI
Blood pressure
Smoking status
PMH (Migraine, VTE, cancer, CVD, SLE)

299
Q

What is a missed pill?

A

When pill is more than 24 hours late, so 48 hours since last pill

300
Q

Advice around missed pills when taking COCP?

A

Missing one pill within 72 hours;
Take missed pill ASAP
No extra protection if other pills taken correctly

Missing more than 1 pill and more than 72 hours since last pill;
Take missed pill ASAP
Additional contraception for 7 days

Consider emergency contraception

301
Q

When should pill be stopped for medical reason?

A

4 weeks before planned surgery

302
Q

What reduces efficacy of COCP?

A

Vomiting
Diarrhoea
Medications like rifampicin

303
Q

Efficacy of POP?

A

99% with perfect use, 91% with typical use

304
Q

UKMEC4 contraindication for POP?

A

Active breast cancer

305
Q

Difference between traditional POP and cerazette?

A

Missed pill window is 3 hours in traditional pill compared to 12 hours in cerazette

306
Q

Mechanism of action of traditional POP?

A

Thickens cervical mucus
Makes endometrium less favourable for implantation

307
Q

Mechanism of action of desogestrel?

A

Inhibits ovulation
Thickens cervical mucus
Alters endometrium
Reduced ciliary action in fallopian tubes

308
Q

When should POP be commenced?

A

Day 1-5; immediate protection

Any other time requires 48 hours

309
Q

Best time to switch from COCP to POP?

A

Day 1-7 of hormone free period

310
Q

Side effects of POP?

A

Amenorrhoea
Irregular prolonged bleeding
Breast tenderness
Headache
Acne

Risk of ovarian cysts, Breast cancer

311
Q

Management of missed pills when taking POP?

A

Extra contraception for 48 hours
Emergency contraception is UPSI within 48 hours

Vomiting and diarrhoea accounts for missed pill

312
Q

What is in the Progesterone only injection?

A

Medroxyprogesterone acetate

313
Q

Efficacy of DMPA?

A

99% with perfect use and 94% with typical use

314
Q

How long does it take for fertility to return following DMPA?

A

12 months

315
Q

Preparations of Progesterone only injection?

A

Depo provera; IM injection
Sayana press; SC self injection

Noristerat; norethisterone containing preparation that works for 8 weeks

316
Q

Contraindications to progesterone only injection?

A

UKMEC4; Active breast cancer

UKMEC3;
Ischaemic heart disease
Unexplained vaginal bleeding
Severe liver cirrhosis
Liver cancer

UKMEC2;
Over 45 years and should switch to another form by 50

DMPA causes osteopororsis so caution in women on corticosteroids for asthma, inflammatory condition

317
Q

Timing of progesterone only injection and insertion of implant?

A

Day 1-5 of cycle provides immediate protection

After day 5 requires 7 days of extra contraception

Injection every 12-13 weeks

318
Q

Side effects of progesterone only injection?

A

Irregular bleeding
Weight gain
Acne
Reduced libido
Mood changes
Headaches
Flushes
Flushes
Hair loss
Skin reaction to injection site
Reduced bone mineral density

319
Q

Benefits of progesterone only injection?

A

Improves dysmenorrhoea
Improves endometriosis symptoms
Reduces risk of ovarian and endometrial cancer
Reduces severity of sickle cell crisis

320
Q

How long does progesterone only implant last?

A

3 years

321
Q

Efficacy of progesterone implant?

A

99%

322
Q

Which progesterone implant is licensed in the UK and what dosage?

A

Nexplanon containing 68mg of etonogestrel

Licensed for use in 18 to 40 year olds

323
Q

Mechanism of progesterone only injection and implant?

A

Inhibits ovulation
Thickens cervical mucus
Alters endometrium

324
Q

Where is progesterone implant inserted?

A

1/3 way up upper arm on the medial side

325
Q

Benefits of progesterone implant?

A

Effective and reliable contraception
Improve dysmenorrhoea
Makes periods lighter or stop completely
Does not cause weight gain
Does not affect bone mineral density
No increase in risk of thrombosis

326
Q

Drawbacks from using progesterone implant?

A

Minor operation to insert and remove
Worsen acne
No protection against STI
Can cause problematic bleeding
Implants can be bent or fractured or impalpable

327
Q

How is prolonged bleeding managed when taking progesterone only contraception?

A

COCP

328
Q

Contraindication to coils?

A

PID
Immunosuppression
Pregnancy
Unexplained bleeding
Pelvic cancer
Uterine cavity distortion

329
Q

Risks related to coil insertion?

A

Bleeding
Pain on insertion
Vasovagal reactions
Uterine perforation
PID in first 20 days
Expulsion

330
Q

Advice prior to removing coil?

A

Abstain from sex 7 days prior to removal

331
Q

Causes of non visible coil thread?

A

Expulsion
Pregnancy
Uterine perforation

332
Q

Management of non visible coil thread?

A

USS, pelvic Xray
Hysteroscopy or laparoscopy

333
Q

Mechanism of copper coil?

A

Toxic to sperm
Makes endometrium less acceptable to implantation

334
Q

Benefits of copper coil?

A

Reliable
Inserted at any time and effective immediately
No hormones
Reduces risk of endometrial and cervical cancer

335
Q

Drawbacks of copper coils?

A

Procedure to insert coil carries risks
Heavy intermenstrual bleeding
Pelvic pain
Does not protect against pelvic pain
Increased risk of ectopic pregnancy
Expulsion1

336
Q

Types of levonorgestrel systems?

A

Mirena; 5 years, licensed for mennorhagia, HRT
Levosert; 5 years, mennorhagia
Kyleena; 5 years
Jaydess; 3 years

337
Q

What is ALO?

A

Actinomyces like organisms observed on smear tests in women using coils require no treatment unless symptomatic where consider taking coil out

338
Q

Benefits of IUS?

A

Makes periods lighter or stop altogether
Improve dysmenorrhoea
No effect on bone mineral density
No risk of VTE
No restrictions in obese patients
Mirena has additional uses

339
Q

Drawbacks of IUS?

A

Procedure to insert
Pelvic pain
Does not protect against STI
Increased risk of ectopic pregnancy, ovarian cyst,
Systemic absorption can lead to acne, headache, breast tenderness

340
Q

Options for emergency contraception?

A

Levonorgestrel- 72 hours of UPSI
Ulipristal- within 120 hours of UPSI
Copper coil- within 5 days of UPSI or within 5 days of estimated

341
Q

Gold standard emergency contraception?

A

Copper coil as it is not affected by BMI, enzyme inducing drugs, malabsorption

342
Q

What is ulipristal?

A

Selective progesterone receptor modulator which works by delayed ovulation

343
Q

Side effects of ulipristal?

A

Nausea, vomiting
Spotting and changes to next menstrual period
Abdominal/ pelvic pain
Back pain
Mood changes
Headache
Dizziness
Breast tenderness

344
Q

Restriction when taking ulipristal?

A

Avoid breast feeding for 1 week
Avoid in severe asthma

345
Q

Types of sterilisation procedures?

A

Tubal occlusion using filshie clips or tubal ties

Vasectomy

Phase 3A (7 decks)

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