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year 3 > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

What speculum is used when examining pelvic organ prolapse

A

Sim’s

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2
Q

What is the uterus divided into

A

Corpus and cervix uteri

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3
Q

What shape is the uterus in most women

A

Anteverted

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4
Q

How long are fallopian tubes

A

10 cm

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5
Q

How is the fallopian tubes divided

A

Isthmus
Infundibulum
Ampulla

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6
Q

What does the uterine artery branch off from

A

Internal iliac

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7
Q

How is the uterus drained venous

A

internal iliac vein

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8
Q

Right vs left ovary venous drainage

A

Right - IVC

Left: Left renal vein

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9
Q

Where do ovarian arteries branch from

A

Abdominal aorta under renal artery

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10
Q

Blood supply of vagina

A

Vaginal artery
Inferior vesical artery
Clitoral branch of pudendal artery

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11
Q

Peritoneal coverage of ureters

A

Retro

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12
Q

Blood supply of bladder

A

Superior and inferior vesicle arteries (internal iliac artery)

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13
Q

Blood supply of rectum

A

Superior, middle and inferior rectal arteries (inferior mesenteric, internal iliac and peudendal arteries)

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14
Q

Lymphatic drainage of ovaries, cervix and endometrium

A

Para-aortic nodes

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15
Q

Types of FGM

A

1: Sunna - removal of prepuce with or without part or entire clit
2. Clitoridectomy with partial or total excision of labia minor
3. Removal of part or all external genitalisa with narrowing of vaginal canal.

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16
Q

Immediate complications of FGM

A
  1. Shock and pain
  2. Haemorrhage
  3. Organ damage
  4. Acute urinary retention
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17
Q

Long-term complications of FGM

A
  1. Recurrent UTI
  2. Urethral obstruction
  3. Pelvic infection
  4. Sexual dysfunction
  5. HIV.AIDS
  6. Pregnancy
  7. Depression
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18
Q

How is FGM sexual dysfunction treated

A
  1. De-infibulation under GA
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19
Q

How is FGM obstructed labour or tears/urethral injury treated

A

De-infibulation during second stage of labour under LA

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20
Q

What is de-infibulation

A
  1. Surgical technique to open the vagina
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21
Q

What causes malformation of the genital tract

A

Failure of paramesonephric ducts to form:

Complete - Rokitansky syndrome

Partial - unicornuate uterus

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22
Q

Signs and symptoms of Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome

A

Painless primary amenorrhoea, normal secondary sexual characteristics, blond ending or absentt vagina

Rokitansky: Vaginal dilation

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23
Q

Signs of imperforate hyman

A

Clinical pain
Primary amenorrhoea
Blush bulging
Memorane visible at introitus

Treatment: Cruciate incision in obstructive membrane

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24
Q

Signs of transverse vaginal septum

A

Clinical pain
primary ammoenorhea
Abdo mass + urinary retention

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25
Q

Signs of longitudinal vaginal septa and rudimentary uterine horns

A

Dyspareunia
Abdo mass

Treatment: Surgical vaginoplasty

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26
Q

What week does gender become apparent during development

A

12th week

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27
Q

What structures form in 6th week of life

A
  1. Genital ridges (induced by primordial germ cells of yolk sack)
  2. Medonephic ducts
  3. Paramesonpephci ducts
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28
Q

What do the paramesonephric ducts develop into

A
  1. Fallopian tubes
  2. Uterus
  3. Cervix
  4. Upper 4.5 of vagina
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29
Q

What structure forms the lower 1/5 of the vagina

A

sinovaginal bulbs of the urogenital sinus, which fuses with the paramesonephric ducts

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30
Q

What do the muscles of the vagina and uterus develop from

A

Mesoderm

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31
Q

What gene causes development of male genitalia

A

SRY gene - produces anti-mullerian hormone

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32
Q

Investigations of genital tract malformation

A
  1. MRI - GOLD
  2. Karyotyping to exclude androgen insensitivity syndrome e
  3. Vaginoscopy
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33
Q

Pathophysiology of 46XX Karyotypee

A
  1. Congenital adrenal hyperplasia

2. Causes hermaphroditism

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34
Q

Pathophysiology of 46XY Karyotype

A
  1. AIS

2. Defects in testosterone biosynthesis (5 alpha reductase, 17 betahydroxysteroid dehydrogenase deficiency)

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35
Q

What is congenital adrenal hyperplasia

A
  1. recessive

Cortisol deficiency causes increased ACTH secretion and androgen production

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36
Q

What causes congenital adrenal hyperplasia

A

21-hydroxylase deficiency

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37
Q

Signs of CAH

A
  1. Neonatal salt wasting crisis
  2. Hypoglycaemia
  3. Childhood virilization and accelerated growth with restricted final height due to early epiphyseal closure
  4. Hirstiusm and oligomenorrhoea
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38
Q

Management of CAH

A
  1. Glucocorticoid (dexamtheasone) to suppress ACTH

Remember - risk for iatrogenic cushion’s syndrome

  1. Salt-losing - fludrocortison to replace aldosterone
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39
Q

What causes androgen insensitivity syndrome

A
  1. Mutation in androgen receptor gene causing resistance to androgens in target tissues
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40
Q

Clinical features of AIS

A
  1. External female genitalisa
  2. Absent uterus and fallopian tubes
  3. Breast development
  4. Sparse pubic hair
  5. Short blind-ending vagina

Can also be very mild (e.g. not present oil puberty when they have a high-pitched voice and gynaecomastia)

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41
Q

Management of AIS

A
  1. Gonadectomy
  2. HRT with oestrogen
  3. Check bone mineral density
  4. Psychological intervention
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42
Q

Management of AIS

A
  1. Gonadectomy
  2. HRT with oestrogen
  3. Check bone mineral density
  4. Psychological intervention
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43
Q

Where is CRH produced

A

Hypothalamus

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44
Q

Where is ACTH produced

A

Pituitary glands

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45
Q

Where does ACTH act

A

Adrenal cortex - fasciulata

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46
Q

Three layers of adrenal cortex

A
  1. Zona glomerulosa
    Fasciulata
    Reticularis
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47
Q

What is produced in the fasciulata

A

Glucocorticoids - lipid soluble has to be bound to a protein in the blood to be transported

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48
Q

Role of cortisol

A
  1. Iridium rhythm
  2. Maintain BP by increasing sensitivity to catecholamines
  3. Supress immune system by reducing inflammatory mediators
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49
Q

Exogenous vs endogenous cushings

A
  1. EXO - by drugs
  2. ENDO - by body

Causes atrophy of the adrenal glands by stopping producing f ACTH

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50
Q

What drugs can cause cushings

A
  1. Prednisolone
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51
Q

What is endogenous cushing caused buy

A

Pituitary adenoma - causes excess ACTh production

Causes yperpalasia of adrenal glands

Tumours of adrenal glands - causes cells of fascilulata to rapidly divide

suppresses CRH and ACTH but cells continue to secrete cortisol production

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52
Q

Ectopic sources of ACTH

A

Small cell lung cancer

Bronchial carcinoids

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53
Q

Symptoms of cushion’s

A
  1. destroys superficial layers of body

Muscle wasting, thin extremities and skin thinning, easy bruising and abdo striae

Osteoporosis

Increased blood glucose due to increased gluconeogenesis - insulin resistance

Moon shaped face

Buffalo hump

Fat redistribution

Arterial hypertension: catecholamine effect

Increased BP by working as aldosterone

Inhibits secretion of GnRH - amenorrhoea

Increased ACTh causes increased androgen - Hirsutism

Immunosuppression

Impair brain function

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54
Q

Diagnosis of cushings

A

24 hr urine free cortisol

Blood or saliva tests at midnight

Dexamthetsone suppression tests - surpasses ACTh production -> serumcortisol unchanged should go down

if pos: ACTH plasma levels:

low - adrenal tumours

high - cushing disease

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55
Q

Diagnosis of cushings

A

24 hr urine free cortisol

Blood or saliva tests at midnight

Dexamthetsone suppression tests - surpasses ACTh production -> serumcortisol unchanged should go down

if pos: ACTH plasma levels:

low - adrenal tumours

high - cushing disease

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56
Q

What is precocious puberty

A
  1. Signs of puberty before 8 or menarche before 10
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57
Q

Problem of precocious puberty

A

Accelerate linear growth with premature epiphyseal closere

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58
Q

Causes of precocious puberty

A
  1. Idiopathic
  2. hypothyroidism
  3. Ovarian cyst
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59
Q

Investigation for precocious puberty

A
  1. Bone age
  2. Cranial MRI
  3. Pelvic USS
  4. FSH/LH/17hydroxyprogesterone
  5. TFTs
  6. GNrH stimulation test
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60
Q

Treatment of precocious puberty

A
  1. GnRH analogue
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61
Q

What are the tanner stages

A

Female:

B1 - Prepubertal
B2 - Breast Bud
B3 - Juvenile with smooth counter
B4 - Areola and papilla project above breast
B5 - Adult

Male:

G1 - Prepubertal, testicular volume <1.5 ml
G2 - Penis grows in length, volume (1.5-1.6)
G3 - Penis grows further in length and circumference, testicular volume (6-12 ml)
G4 - Development of glans penis, darkening of scrotal skin + testicular volume (12-20ml)
G5 - Adult genitalia, testicular volume > 20ml

Pubic Hair:
PH1 - None
PH2 - Sparse at the base
PH3 - Dark, coarser
PH4 - Filling out towards adult distribution
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62
Q

What defines delayed puberty

A
  1. Absence of menstruation and secondary sexual characteristics by 14
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63
Q

Causes of delayed puberty

A
  1. Weight loss
  2. Hypothalamic disorders
  3. varian failure
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64
Q

Investigations for delayed puberty

A
  1. LH/FSH/testosterone/TFTs/Prolactin
  2. Karyotype
  3. Pelvic ultrasound/MRI if mullein anomaly suspected
  4. Cranial MRi if prolactin is high
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65
Q

What is vulvovaginitis + treatment

A
  1. Starts when girl becomes responsible for going toilet

T: Wiping front to back
Loose cotton underwear
Emollient

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66
Q

Differential for vulvovaginitis

A

Sexual abuse

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67
Q

What causes labial adhesions

A
  1. Hypo-oestrogenic state
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68
Q

What is lichen sclerosus + treatment

A

Sticky, white plaques in butterfly patter around anogenital area - sparing of vagina

Signs:

Dysuria, surface bleeding and purport from itching

T: Topical corticosteroids

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69
Q

Target BP in clinic and ABPM/HBPM

A

clinic; 140/90

ABPM: 135/85

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70
Q

HbA1c target with lifestyle and metformin

A

48 mol/mol (6.5%)

target is 53 on sulfonylurea

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71
Q

Drug treatment of T2DM

A

Metformin

Metformin + Glisten/sulfonylurea/pioglitazone/sglt-2 inhibitor

then triple therapy of above

Re-visit diabetes on osmosis

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72
Q

When should double therapy start

A

if hba1c is over 58 mol/mol

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73
Q

Signs of hypercalcaemia

A 
Stones (renal)
Bones (pain)
Groans (also pain, nausea and vomiting)
Thrones (polyuria)
Psychiatric overtones
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74
Q

Characteristic x ray finding in hyperparathyroidism

A

Pepperpot skull

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75
Q

Most important complication of fluid rests in DKA

A

Cerebral oedema (Raised glucose and ketones)

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76
Q

Treatment of MODY diabetes (HNF1A)

A

Gliclazide - sulfonylureas

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77
Q

What can ovarian cysts be divided into

A

Simple or COmplex

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78
Q

What types of simple cysts are there

A

Follicular cyst: Dominant follicule fails to rupture / Normal surge of LH doesn’t happen

This is the MOST common ovarian mass in young individuals

Corpus Luteum cyst

Theca Lutein Cyst

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79
Q

What is polycystic ovary syndrome

A

multiple follicular cysts

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80
Q

What causes PCOS

A
  1. Chronic anovulation

Dysfunction in hypothalamic-pituitary-ovarian axis.

This causes amenorrhoea and excess androgen production (hirsutism)

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81
Q

What causes a corpus luteum cyst (haemorrhgaic cyst)

A

Instead of regressing, it continues to grow

The ruptured follicle begins producing large quantities of estrogen and progesterone in preparation for conception. If a pregnancy doesn’t occur, the corpus luteum usually breaks down and disappears. It may, however, fill with fluid or blood, causing the corpus luteum to expand into a cyst, and stay in the ovary.

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82
Q

How can we distinguish between a corpus luteum cyst and other cysts

A

Appears as an enlargement of the ovary itself instead of a mass

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83
Q

What causes a theca lutein cyst

A

Overstimulation of hCG (ONLY SEEN IN PREGNANCY)

Stimulates growth of follicular theca cells on both OVARIES

Thus, bilateral cysts (REMEMBER THIS) during pregnancy

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84
Q

When is theca lutein cyst more likely to develop

A
  1. Multiple foetuses

2. Gestational trophoblastic disease

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85
Q

What is gestational trophoblastic disease

A

pregnancy-related tumours. These tumours are rare, and they appear when cells in the womb start to proliferate uncontrollably. The cells that form gestational trophoblastic tumours are called trophoblasts and come from tissue that grows to form the placenta during pregnancy.

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86
Q

Diagnosis of gestational trophoblastic disease

A

Check for serum beta hCG.

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87
Q

4 Characteristcics of a complex cyst

A
  1. Large
  2. Irregular borders
  3. Internal septations (multilocular)
  4. Fluid is heterogenous (something other than just fluid inside it)
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88
Q

Name the three types of ovarian tumours

A
  1. Epithelial ovarian tumours (from surface epithelium of ovaries)
  2. Germ cell (from primordial germ cells)
  3. Sex Cord-stromal (from connective tissue of ovaries)
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89
Q

Most common ovarian tumour

A

Epithelial ovarian

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90
Q

4 Types of epithelial ovarian tumours

A
  1. Serous (cystic)
  2. Mucinous
  3. Endometrioid
  4. Transitional

They can either be benign, malignant or borderline

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91
Q

Histology of serous/mucinous cyst adenoma

A

Single cost with simple cuboidal and columnar cells.

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92
Q

What group of women are most likely to have serous/mucinous cystasenoma

A

Premenopausal women (30-40)

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93
Q

Characteristics of serous vs mutinous cyst adenoma

A

Serous: bilateral and fallopian tube-like epithelium

CONTAIN PSAMMOMA BODIES (calcium deposits around dead cells)

Mucinus: Unilateral
Mucus secreting epithelium (columnar)

Pseudomyxoma Peritonei

Ends up leaking into the appendix or GI - metastases

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94
Q

What characterises borderline tumours

A

Mix of characteristics from benign and malignant types but have bette outcomes than malignant (less likely to metastasise)

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95
Q

What cells do epithelial ovarian tumours arise from

A

Usually called ENDOMETRIOMAS (so from endometrial cells)

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96
Q

What causes endometriomas

A

Benign cysts that occur in endometriosis (endometrial tissue from uterus grown on ovary).

Endometrial tissue responds to hormones -> bleeds within cavity during menstruation (CHOCOLATE CYSTS as blood turns dark)

Once these rupture, the contents spill inside peritoneal cavity

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97
Q

What are entometrioids tumours made of

A

Type of malignant endometriadenomas ovarian tumour that is composed of endometrial-like glands

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98
Q

What type of ovarian tour are brenner tumours

A

Benign Epithelial Ovarian tumour made form transitional cells

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99
Q

Histology of Brenner tumours

A

Coffee bean shaped

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100
Q

What can brenner tumours transition to

A

Squamous cell carcinoma

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101
Q

4 Types of germ cell tumours

A

Fetal
Oocyte
Yolk Sac
Placenta

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102
Q

What are teratomas

A

Tumours that arise from fetal tissue

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103
Q

What are the two types of teratomas

A
  1. Mature Cystic Teratoma (dermoid cyst)

2. Immature Teratoma

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104
Q

What is composed of a mature cysts teratoma

A
  1. Skin, Hair, Nails etc (fully developed tissue)

2. Stroma Ovarii

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105
Q

What is the most common ovarian tumour in females (10-30)

A

Mature cystic teratoma

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106
Q

Characteristics of mature cystic teratoma

A
  1. Benign (sometimes can progress to squamous cell carcinoma)
  2. Usually unilateral

Important to look at age

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107
Q

What is stroma Ovari

A

ONLY CONTAINS THYROID TISSUE

These secrete T2 and T4 - hyperthyroidism

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108
Q

Important signs for stroma ovarii

A

Normal thyroid exam
Low TSH
Ovarian Mass

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109
Q

What is an immature teratoma

A

Undifferentiated fetal tissue (neuroectoderm)

MALIGNANT AND VERY AGGRESSIVE

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110
Q

What age onset is immature teratoma

A

Less than 20

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111
Q

What are oocyte germ cell tumours called

A

Dysgerminomas (most common malignant germ cell tumours) - adolescent

These are ovarian analogues of testicular seminomas

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112
Q

Histology of dysgerminomas

A

Fried-Egg Appearance

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113
Q

What are markers for Dysgerminomas

A

LDH
hCG

These tend to be abundant in the tumour cells

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114
Q

What is the tumour of the yolk sac called

A

Endodermal sinus tumour - MALIGNANT

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115
Q

In what patients are endodermal sinus tumours (yolk sac) most common

A

Children

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116
Q

Sign of endodermal sinus tumour on physical exam

A

Yellow Haemorrhagic mass

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117
Q

Histology of endodermal sinus tumours

A

Schiller-Duval Bodies (malignant cells surround central blood vessels)

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118
Q

Lab results for endodermal sinus tumour

A

Increased alpha fetoprotein (AFP)

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119
Q

What are placental germ cell tumours called

A

Choriocarcinoma (Can sometimes happen in ovaries)

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120
Q

Histology of Choriocarcinoma

A
  1. Cytotrophobblasts
  2. Syncytiotrophoblast

BUT NO VILLI unlike placental tissue

High chance of bleeding and spreading via circulation

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121
Q

Cytotropholoblasts vs syncytiotrophoblast

A

Cato - light cytoplasm and uninuclei

Syncytio - dark cytoplasm and multiple nuclei

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122
Q

Lab results for choriocarcinoma

A
  1. High hCG levels
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123
Q

What is the alpha subunit of hCG levels similar to

A

TSH and thus stimulates TSH levels - causing hyperthyroidism

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124
Q

Symptoms of choriocarcinoma

A
  1. Heat Intolerance
  2. Sweating
  3. Palpitations
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125
Q

Signs for choriocarcinoma

A
  1. Hyperthyroidism
  2. Normal thyroid
  3. Ovarian Mass
  4. High hCG levels
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126
Q

Four subtypes of Sex cord-stomal tumours

A

Granulose Cell Tumours
Thecomas
Fibromas
Sertoli-Leydig tumours

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127
Q

Where do sex cord-stomal tumours arise from

A

Connective tissue of ovaries

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128
Q

What is the most malignant type of sec cord-stomal tumour

A

Granulose cell tumour

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129
Q

Histological appearance of granulose cell tumour

A
  1. Call-Exner Bodies

Granulose-like cells surrounding eosinophilic fluid

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130
Q

Marker for granulose cell tumours

A

Raised Inhibin B - produced by granulosa cells.

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131
Q

What are thecfmas mad elf

A

BENGIN

Made of Theca Cells

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132
Q

In what women are granulose and theca cell tumours common

A

POSTMENOPAUSAL WOMEN

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133
Q

Lab results of granulose and theca cell tumours

A

Excessive oestrogen secretion:

Weight Gain
Breast Tenderness
Irregular Menses
Menorrhagia

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134
Q

What are fibromas made of

A

Bundles of fibroblasts - BENIGN

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135
Q

What is Meigs Syndrome

A
  1. Ascites
  2. Hydrothorax

Fibromas

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136
Q

What are contained in Leydig Cells

A

Reinke crystals

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137
Q

Lab results for Sertoli-Leydig tumours

A
  1. Secrete androgens (testosterone)

Thus, symptoms include acne, hirsutism, deeper voice, hair loss.

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138
Q

What tumours are bilateral

A

theca lutein cyst

Krukenberg tumour

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139
Q

Where do krukenberg tumours come from

A

GI system: Diffuse gastric carcinoma

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140
Q

Histology of krukenberg cells

A

Signet ring cells (vacuole with mucin and nucleus)

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141
Q

Risk factors for ovarian cancer

A
  1. Less ovulation cycles = lower risk (less cell division):
    Having kids
    Breast feeding
    Contraceptives
2. More cycles: 
No pregnancy
Infertility
Early Menarche
Late menopause
Endometriosis 
PCOS
  1. BRCA-1 or 2 mutation
  2. Endometrial/colon/GI cancer in family
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142
Q

Symptoms of Ovarian cancer

A
  1. Change in bowel habits
  2. Pelvic discomfort (pulling sensation in groin)
  3. Bloating
  4. Dull/aching lower abdominal pain
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143
Q

What are ovarian torsions

A

Ovary twists around suspensory ligament.

Causes sudden, sharp and acute pelvic pain (cuts of blood supply)

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144
Q

Symptoms of PCOS and sertoli-leydig cell tumours

A
  1. Amenorrhoea
  2. Acne
  3. Hirsutism
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145
Q

Symptoms of endometriomas

A
  1. Dysmenorrhoea (pain)

2. Fertility issues

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146
Q

Symptoms of strums ovary and choriocarcinoma

A
  1. Hyperthyoridism
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147
Q

Symptoms of granulose and theca cell tumours

A
  1. Oestrogen excess

Precocious puberty (before 8)

Mennorhagia and menorrhagia

Menopausal - Uterine bleeding

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148
Q

Signs of metastasise

A
  1. Ascites
  2. Abdo mass
  3. Abdo distention
  4. Bowel obstruction
  5. Pleural effusion
  6. Sister Mary Joseph nodules (nodes around umbilicus) - usually indicative of gastric cancer
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149
Q

Diagnosis of Ovarian cancer

A
  1. Pelvic exam
  2. Blood test (LDH, beta-HCG, AFP and Inhibin B)
  3. Imaging: Transvaginal/Abdo ultrasound
  4. CT/MRI of pelvis

GOLD STANDARD - Biopsy

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150
Q

Tumour marker to gage efficacy of chemotherapy

A

Carbohydrate antigen 125.

Not specific enough for diagnosis or screening

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151
Q

Adverse effect of cancer therapy on Ovaries, Uterus and hypothalamus

A
  1. Ovarian failure
  2. Reduced uterine function
  3. Hypogonadotrophic hypogonadism
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152
Q

What is the follicular phase of the menstrual cycle

A
  1. Pulsatile release of hypothalamic GnRH -> FSH from anterior pituitary gland
  2. FSH promotes ovarian follicular development -> recruitment of a dominant follicle containing oocyte
  3. Follicular garnulosa cells produce oestrogen (endometrial proliferation)
  4. Increased Oestrogen levels to stop further FSH production
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153
Q

What does oestrogen inhibit

A

FSH

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154
Q

What happens to cause ovulation

A
  1. Increasing follicle oestrogen from positive feedback vita activin
  2. LH surge 36 hours before ovulation
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155
Q

Stages of the luteal phase

A
  1. The follicle collapses down to become corpus luteum
  2. Progesterone and oestrogen act on oestrogen primed endometrium to induce secretory changes (thickens and increased vascularity)
  3. Corpus luteum turns into corpus albicans after 14 days.
  4. if implantation occurs, hCG keeps CL maintained (progesterone continues secretion to support endometrium)
  5. Pregnancy absence causes CL degeneration (rapid fall in progesterone and oestrogen -> menstruation)
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156
Q

What does the corpus luteum produce

A

Oestrogen and progesterone

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157
Q

What days do ovulation occur

A

14-18 days

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158
Q

What days does the corpus luteum develop

A

20-26

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159
Q

What protein causes GnRH to be secreted

A

Kisspeptin

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160
Q

What stimulates the production of Estradiol

A

LH and FSH acting on eggs to produce it

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161
Q

Role of estradiol

A

Proliferation of endometrium

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162
Q

How does the fertilised oocyte maintain the endometriumm

A

Develops in fetus:

Fetal hCG maintains ovarian production of progesterone and placental progesterone

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163
Q

Where is progerstone produced

A

Adrenal Cortex

Ovarian corpus luteum

Placenta later on

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164
Q

Where is oestrogen produced

A

Ovaries (theca interna)

Placenta when pregnant

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165
Q

How long is the menstrual cycle

A

28 Days

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166
Q

When does LH production start and end

A

12-14

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167
Q

What causes variation in ovulatory cycles

A

The follicular phase (luteal phase is fixed)

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168
Q

Average menstruation (bleeding days)

A

3-5 days

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169
Q

What is Oligomenorrhoea

A
  1. When cycles last longer than 32 DAYS
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170
Q

Causes of oligomenorrhoea

A
  1. PCOS
  2. Low BMI
  3. Hyperprolactinaemia and mild thyroid disease
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171
Q

Management for dysmenorrhoea

A
  1. STI screen
  2. USS
  3. Laparoscopy
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172
Q

Management of dysmenorrhoea

A

Symptom control:

  1. Mefenamic Acid (500mg)
  2. Paracetamol, hot water bottles, B1 and mg

Treat underlying causes

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173
Q

How is dysfunctional uterine bleeding diagnosed

A
  1. Exclusion, any abnormal uterine bleeding in absence of pathology or pregnancy

(> 80mL)

Usually menorrhagia

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174
Q

Treatment of DUB

A
  1. Tranexamic (controls bleeding) and mefenamic acid (NSAID)

Endometrial ablation

  1. IUS (delivers measured doses of levonorgestrel)
  2. NSAID: Medenamic acid
  3. COCP to regulate cycle
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175
Q

5 reasons for pregnancy termination under law (ABCDE

A

A: Continuance would be a greater risk to pregnant woman’s life than termination
B: Termination will prevent permanent injury physical or mental health
C: Has not exceeded 24 weeks and continuance would cause physical and mental health injuries
D: Pregnancy has not exceeded 24th week and continuance would have physical and mental health risks
E: Substantial risk if child was born

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176
Q

Surgical termination 7-13wks

A

Conventional suction termination

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177
Q

Surgical termination greater than 13 eeks

A

Dilatation and evacuation following cervical prep

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178
Q

Risk with dilatation and evacuation

A

Greater gestation = higher risk of bleeding

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179
Q

What cervical prep should be given

A
  1. Misoprostol
  2. Gemeprost
  3. Mifepristone
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180
Q

Medical intervention for abortion

A

Mifepristone

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181
Q

What is the mifepristone

A

Anti progesterone -? causes uterine contractions, blessing from placental bed and sensitises uterus to prostaglandins

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182
Q

What is misoprostol

A

Prostaglandin E1 analogue -> uterine contractions

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183
Q

What is gemeprost

A

Prostaglandin E1 analogue - softens and dilates cervix

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184
Q

Prophylaxis for TOP

A

Metronidazole + Doxy/azithromycin

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185
Q

Complications of TOP

A

1 .Significant bleeding

  1. UTI
  2. Cervical trauma
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186
Q

4 pathologies to consider in early pregnancy bleeds

A
  1. Miscarriage
  2. Ectopic pregnancy
  3. Gestational trophoblastic disease
  4. Chlamidyia
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187
Q

Define miscarriage

A

Defined as the expulsion of a pregnancy, embryo, or fetus at a stage of
pregnancy when it is incapable of independent survival BEFORE 20 weeks of pregnancy

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188
Q

When do miscarriages usually occur

A

12 weeks

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189
Q

Symptoms of a threatened, complete or incomplete miscarriage

A
  1. Bleeding
  2. Abdo pain
  3. Closed cervic (incomplete right be open)
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190
Q

USS findings for threatened miscarriage

A
  1. Inauterine gestation sac
  2. Fetal pole
  3. Fetal Heart activity
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191
Q

Management for threatened miscarriage

A
  1. Anti-D if >12 weeks or heavy bleeding/pain
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192
Q

USS findings for complete miscarriage

A
  1. Empty Uterus

2. Endometrial thickness (<15 mm)

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193
Q

Management of complete miscarriage

A
  1. Anti - D (> 12 weeks)

2. Serum hCG

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194
Q

USS findings in incomplete miscarriage

A
  1. Uterine contents pass through open cervix
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195
Q

Management of incomplete miscarriage

A
  1. Anti - D and surgery
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196
Q

Symptoms of missed miscarriage

A
  1. Bleeding
  2. Pain
  3. Closed cervix
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197
Q

USS finding of missed miscarriage

A
  1. Fetal pole > 7mm
  2. No fetal heart activity
  3. Mean gestation sac diameter >25 mm with no fetal pole or yolk sac
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198
Q

Symptoms of inevitable miscarriage

A
  1. Bleeding + pain
  2. Open cervix
  3. Uterine contents visible during pelvic exam
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199
Q

USS finding of inevitable miscarriage

A
  1. Inauterine gestation sac
  2. Fetal Pole
  3. Fetal Heart Activity
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200
Q

USS finding of pregnancy of unknown location

A
  1. Positive pregnancy test
  2. Empty uterus
  3. No sign of extrauterine pregnancy
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201
Q

Management of PUL

A
  1. Serum hCG assay and initial serum progesterone to exclude ectopic
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202
Q

How can chromosomal abnormality cause miscarriage

A

ANEUPLOIDY (Extra or missing chromosomes)

Polyploidy (where a zygote receives more than 1 set of 23 chromosomes) 69 or 92 chromosomes

Translocation (Unbalanced exchange of DNA so one might have too much or too little dna)

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203
Q

What condition is caused by Monosomy

A

Turner’s

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204
Q

If the zygote is genetically viable, what is the next cause of a miscarriage (think about the cycle)

A
  1. Blastocyst is unable to implant on the endometrium - no blood supply
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205
Q

What causes an ectopic pregnancy

A
  1. When blastocyst ends up implanting onto other tissues before reaching the uterus (e.g. the fallopian tube)
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206
Q

Why are ectopic pregnancies likely to end in miscarriage

A
  1. No space

2. No blood supply

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207
Q

What is the next cause of miscarried blastocyst implantation is successful

A
  1. Coprus luteum may not secrete enough progesterone to continue development of oocyte
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208
Q

What is the next cause of a miscarriage if the corpus luteum successfully secretes progesterone

A
  1. Placenta unable to exchange gases, o2 and glucose
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209
Q

In what stage of pregnancy is the embryonic period

A

3-8 weeks

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210
Q

What can cause a miscarriage during the embryonic period

A
  1. Teratogen damage (birth defects) - medications

Isotretinoin, mercury, alcohol, smoking

Brain and heart develop in this period

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211
Q

How can growing fetes be assessed 10-14 weeks of pregnancy

A
  1. Chorionic villus sampling
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212
Q

What is chorionic villus sampling

A

Needle or catheter used to take a sample of the placenta for genetic analysis

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213
Q

How can growing fetes be assessed 15 weeks of pregnancy

A

Amniocentesis

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214
Q

What is amniocentesis

A
  1. Aspiration of amniotic fluid
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215
Q

Complications of growing fetes assessment

A

Trauma and infection -> miscarriage

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216
Q

What two uterine abnormalities can cause miscarriages

A
  1. Septate uterus

2. Submucosal leiomyoma (fibroid tissue in submucosa that limits space)

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217
Q

What infections can cause miscarriage s

A
  1. Listeria monocytogenes
  2. Cytomegalovirus (+HSV)
  3. Toxoplasma gondii
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218
Q

Risk factors for miscarriages

A
  1. Obesity
  2. Endocrine (Thyroid, DM, PCOS)
  3. APl, SLE (blood clot)
  4. High BP
  5. AGe
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219
Q

What is a septic abortion

A
  1. Happens during incomplete miscarriage - caused by infection
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220
Q

What is a complete miscarriage

A
  1. Uterine cavity is empty + cervix closed
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221
Q

What is a missed miscarriage

A
  1. Fetus is not viable but cervix has not opened - may be asymptomatic
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222
Q

Symptoms of miscarriage

A

‘blood clots’ - placental or fetal tissues
Lower abdo pain
Increased vaginal bleeding

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223
Q

Diagnosis of miscarriage

A
  1. Transvaginal USS
  2. Pelvic exam
  3. HCG levels
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224
Q

Medical intervention for ectopic pregnancy

A
  1. IM Methotrexate

Monitor hCG levels

Surgery: laparotomy (salpingectomy)

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225
Q

Side effects of methotrexate

A
  1. Conjunctivitis
  2. Stomatitis
  3. GI upset
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226
Q

What is a pregnancy of unknown location

A
  1. No sign of intrauterine pregnancy, ectopic or related products of conception but positive pregnancy test (hCG>5UL)
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227
Q

What does <20nmol/l of progesterone mean for the pregnancy

A
  1. Likely to fail
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228
Q

If rise in hCG<66%, what does this mean for the pregnancy or >1500 IU/L

A

Possibly ectopic

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229
Q

What is beta-hCG secreted by

A
  1. Trophoblasts
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230
Q

What compound is beta-hcg similar to

A

LH

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231
Q

Risk factors for recurrent miscarriage

A

. Ageing
2. APS
Fibroids
Protein C and S deficiency

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232
Q

Management of recurrent miscarriage

A
  1. Pelvic USS
  2. Thrombophilia screening
  3. Lupus anticoagulant
  4. Anticardiolipin antibodies
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233
Q

Life style advice for people with miscarriages

A
  1. Bed Rest
  2. Smoking cessation
  3. Reduce alcohol intake
  4. Losing Weight
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234
Q

What is hyperemesis gravid

A
  1. Excessive vominiting dur to elevated hCG
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235
Q

When does hyperemesis gravid occur

A
  1. 1st trimester
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236
Q

Symptoms of HG

A
  1. VOmiting
  2. Weight loss
  3. Muscle wasting
  4. Dehydration
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237
Q

How to read HG

A

1 .IV fluids

  1. Replace K+
  2. Keep nail by mouth
  3. Promethazine (antiemetics)
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238
Q

Investigations for HG

A
  1. Urinalysis to detect ketonesin urines
  2. MSU to exclude UTI
  3. FBC
  4. U and E
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239
Q

Investigations for HG

A
  1. Urinalysis to detect ketonesin urines
  2. MSU to exclude UTI
  3. FBC
  4. U and E
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240
Q

What does LH act on

A

Theca cells -> produce androstenedione

Granulose cells respond to FSH -> aromatase

This then breaks androstenedione to oestrogen

Oestrogen acts as a negative feedback loop on FSH so only one follicle is stimulated

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241
Q

What happens to the granulose cell once the dominant follicle forms

A

Develops LH receptors so more oestrogen is screwed

-> POSITIVE FEEDBACK so pituitary is more responsive to gnRH - MORE FSH AND LH

These then band to the theca cells to rupture follicle and release oocyte

END OF FOLLICULAR PHASE

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242
Q

What part of the menstrual cycle does cos occur in

A
  1. Follicular
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243
Q

What causes polycystic ovary syndrome

A

Exes LH production causes excess production of androstenedione by theca cells

Excess flows into blood -> estrange by aromatase in fat

Negative feedback prevents LH surge so no follicular destruction. forms a cyst.

Prevents ovulation

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244
Q

Risk factor for PCOS

A
  1. Insulin reisstance - disrupts menstrual cycle

Theca cells have insulin receptors causing them to grow and divide - too many LH receptors

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245
Q

Symptoms of PCOS

A
  1. Excess androstenedione cause hirsutism, male-pattern baldness, acne
  2. lack of ovulation causes amenorhheoa and oligomenorhea
  3. Insulin resistance - Acanthuses nigricans/overweight
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246
Q

PCOS diagnosis

A
  1. LH:FSH ratio
  2. Raised androstenedione
  3. Pelvic USS to look for follicles but not necessary for diagnosis
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247
Q

Treatment of PCOS

A
  1. Wieght loss
  2. Metformin
  3. Spironolactone and contraception as teratogenic
  4. Oral contraceptive to regulate cycle
  5. Clomiphene citrate to induce ovulation
  6. Ovarian drilling to poke the cysts
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248
Q

Symptoms of hirsutism and virilization

A
  1. Weight Gain
  2. Acne
  3. Male Pattern Balding

Virilization: Deepened voice and clitoromegaly

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249
Q

Where can excess androgen production (testosterone) be produced

A
  1. Ovaries

2. Adrenal gland

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250
Q

How can excess hair growth in hirsutism be quantified

A

Ferriman-Gallwey score

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251
Q

What is the Ferriman-Gallway score

A

measures hair in 9 areas:

  1. Upper lip
  2. Chest
  3. Upper bids
  4. Lower abdo
  5. Upper arms
  6. Chin
  7. Upper back
  8. Lower back
  9. Thigh

Graded 0-4
Take into account ethnicity

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252
Q

Score of FGS

A
  1. 8-15 (mild)
  2. 16-25 (moderate)
  3. > 25 (severe)

Asian: > 2

Meditteranaena, middle eastern and latina (only over 10)

Change of hair growth pattern and rate

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253
Q

Ovarian diseases that can cause hirsutism

A
  1. PCOS MAIN
  2. Androgen tumours
  3. Luteoma
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254
Q

Adrenal gland causes of hirsutism

A
  1. CAH
  2. Cushings
  3. Tumours
  4. Acromegaly
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255
Q

What women are more likely to have pcos

A

Premenopausal

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256
Q

Symptoms of PCOS

A
  1. Menstrual irregularities (oligoenorrhoea or amenorhheoa)

2.

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257
Q

What is non-classic congenital adrenal hyperplasia

A
  1. 21-Hydroxylase deficiency

So 17-hydroxyprogesterone ends up as androgens (excess)

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258
Q

Role of 21-hydroxylase

A

Converts 17-hydroxyprogesterone -> 11 deoxycrotisol -> cortisol

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259
Q

What shows on USS TV for PCOS

A
  1. 12 follicles (2-9 mm)

2. Ovarian Volume >10cm^3

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260
Q

Test for PCOS

A
  1. TV USS and serum total testosterone

*>60 ng/Dl
<150ng/dL

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261
Q

PCOS vs CAH

A

17-hydroxyprogesteorne elevated (>200ng/mL)

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262
Q

Test for CAH

A

ACTH stimulation stimulates adrenal hormon production (1500 ng/ml)

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263
Q

Treatment for CAH

A

COCP to reduce hirsutism and cycle regulation

Spironolactone

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264
Q

What drug induces ovulation

A

Clomiphene citrate

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265
Q

Red flags for hirsutism/ virilization

A
  1. Rapidly worsening hirsutism and vilirilzation may be an adrenal and ovarian tumour
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266
Q

Tests for tumours causing virilization and hirsutism

A

Serum Testosterone >150ng/dL

Serum DHEA: <700 is ovarian

> 700 adrenal

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267
Q

Chemo for ovarian tumours

A

Bleomycin, Etoposide and cisplatin

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268
Q

Test for malignant adrenal carcinomas

A
  1. Urinary Metanephrine test

High metanephrine = alpha blockers to prevent hypotensive crisis

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269
Q

Therapy for stage 4 adrenal tumours

A

Mitotane and radiation therapy

Debunking surgery

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270
Q

In what women is ovarian hyperthecosis seen

A

Post-menopausal

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271
Q

Signs of Ovarian hyperthecosis

A
  1. Testosterone > 150ng/dL
  2. Insulin reisstance
  3. Hyperinsulinemia
  4. No cysts on USS TV and physical exam
  5. Increased bilateral ovarian stroma
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272
Q

Treatment for ovarian hyperthecosis

A

Insulin reisstance + want pregancy: Metformin + Clomiphene

Insulin resistance + no pregnancy: COCP + Spironolactone

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273
Q

What is the sole symptom of hirsutism called (nothing else wrong with them, lab results normal)

A

IP hirsutism

Shaving

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274
Q

Treatment for hirstusim

A
  1. Laser and electrolysis
  2. Spironolactone
  3. Cyproterone acetate
  4. Finasteride
  5. Flutamide
  6. Eflornithine hydrochloride
  7. GnRH agonist
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275
Q

Pharmacology of spironolactone

A
  1. Aldosterone antagonist

Stops ovarian and adrenal androgen production

Also inhibits 5-alpha reductase in skin - acne

Can cause hyperkalaemia

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276
Q

Pharmacology of cyproteone acetate

A
  1. Inhibits LH secretion

Can cause oedema, fatigue, weight loss

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277
Q

Pharmacology of finasteride

A
  1. Inhibits 5-alpha reducatese
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278
Q

What is endometriosis

A

Where the endometrial cells grow outwards (outside the womb)

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279
Q

Three layers of threproductive system

A
  1. Perimetric
  2. Myometrium
  3. Endometrium
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280
Q

What happens in endometriosis

A
  1. Cells making up the endometrium migrate to other parts of the reproductive system and start growing to form a mass (ovaries, tubes and uterine ligaments)
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281
Q

What are the 5 main theories that can cause endometriosis

A
  1. Retrograde menstruation theory
  2. Immune system dysfunction (allows cells to grow)
  3. Metaplastic theory (cells of peritoneum transform into endometrial tissue)
  4. Benign metastases theory
  5. Extrauterine stem cell theory

Last two may explain how they show up in lungs and hearts

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282
Q

RF for endometriosis

A
  1. FH
  2. Never been pregnant
  3. Early menarche
  4. Late menopause
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283
Q

Normal endometrial cells vs implanted

A
  1. Implanted: high levels of aromatase to produce oestrogen
  2. Pro-inflammatory factors causing inflammation and scarring (adhesion)

Chronic inflammation and hormone level changes will cause bleeding or endometriomas (choice cysts) on ovaries

284
Q

What genes mutate in endometriomas

A

PTEN
ARID1A

Increases risk of ovarian carcinoma

285
Q

Symptoms of endometriomas

A

Reproductive organs:

  • pelvic pain
  • Bleeding
  • dysmenorrhea
  • dysparaenuia

Pouch of douglas:
- dyschezia (pain in defecation)

Bladder: Painful urination
Intestines: Abdo pain

pain gets worse during periods

tend to be sub fertile due to scarring causing implantation difficulties

286
Q

Diagnosis of endometriosis

A

Laparoscopy

287
Q

Treatment of endometriosis

A
  1. Oetsorgen-progesterone OCP (ovarian suppression
  2. Progesterone analogs (medroxyprogesteroene + levonorgesterol)
  3. Danazol (steroid that inhibits mid cycle surges of FSH and LH
  4. Gonadotropin-releasing hormone modulators tor educe oestrogen levels
288
Q

Surgical treatment of endometriosis

A
  1. Excision of implants

2. Pain is delimitation: oophorectomy or hysterectomy

289
Q

Common sites for endometriosis

A
  1. pouch of douglas
  2. Uterosacral ligaments
  3. Ovarian fosse
  4. Bladder
  5. Peritoneum
290
Q

Appearance of endometriosis

A

choco cyst

291
Q

Examination of endometriosis

A
  1. Pelvic exam and speculum
  2. TV USS
  3. Laparoscopy and biopsy
292
Q

What grading system is used for endometriosis

A
  1. rASRM 1996

Location, size, depth of infiltration, adhesions

Stage I: Minimal endometriosis (1–5 points).
• Stage II: Mild endometriosis (6–15 points).
• Stage III: Moderate endometriosis (16–40 points). • Stage IV: Severe endometriosis (>40 points).

293
Q

How are GnRH analogues admitted

A

SC injection

294
Q

What is Amenorrhoea

A

No menstruation

295
Q

What is primary amenorrhoea

A
  1. Menstruation never starts
296
Q

Three cases in where amenorrheoa is normal

A
  1. Before Puberty
  2. During pregnancy and lactation
  3. After menopause
297
Q

What is the follicular phase

A
  1. Where follicles ‘race’ to become the more dominant mollicule to be released at ovulation
  2. All release oestrogen which suprsses GnRH to rduce FSH and LH production.
298
Q

How long does the menstrual phase last

A

5 Days

299
Q

What is the profilerative phase

A

Follows the menstrual phase where increased in ovarian oestrogen to thicken endometrium layer.

Increased blood supply from spiral artieries to endometrium.

300
Q

What occurs in the luteal phase

A

Occurs after ovulation: where coprus luteum produces progesterone to thicken endometrium:

Spiral arteries continue to grow

If not fertilised: Progesterone and oestrogen levels decrease

301
Q

When are people diagnsoed with Amenorrheoa

A

After age 16 (suspected after 13 with no menarche)

302
Q

Most common cause of primary amenorrheoa

A

Turner Syndrome (45, X) - where one chromosome is completely absent They have 45 instead of 46 chromosomes

secondary cause: Müllerian Agenesis (MRKH syndrome)

Rare: ANdrogen Insensitivity Syndrome and Kallman syndrome

303
Q

What are ovaries replaced by in Turner’s and how is this seen on histology

A
  1. Streak Gonads (functional, fibrous tissues)

Turner’s causes accelerated degeneration of ovarian follicles - menopause before menarche

No Ovarian oestrogen means less inhibition on GnRH = raised LH and FSH

304
Q

What is MRKH syndrome

A

Mullerian ducts responsible for Uterus, cervix, upper 2/3rds vagina do not develop. and are thus, absent or obstructed: absence of menses.

Ovaries develop normally and produces oestrogen so FSH and LH are normal.

305
Q

What is androgen insensitivity syndrome

A

Biologically male (46, XY) but tissues do not respond to testosterone.

No uterus, fallopian tubes or ovaries - menses absent

Have testicales stuck in the ignuinal canal or abdomen which produce testosterone (keeping LH and FSH normal)

306
Q

Consequence of testosterone production by testicles that isn’t binding to tissues in AIS

A
  1. Excess -> converted to oestrogen causing development of female secondary sex characteristics.
307
Q

What is Kallman syndrome

A

Neurons failt o migrate from nose to hypothalamus during fetal development: low levels of GnRH, FSH and LH -> low oestrogen

So puberty never starts or is incomplete.

308
Q

What is secondary amenorrhoea

A

At least 3 menstrual cycles for women who had regular cycles, 6 months for females who had irregular cycles.

309
Q

Most common causes of secondary amenorrheoa

A
  1. Pregnancy
  2. Functional Hypothalamic amenorrheoa - where decreased GnRH secretion causes LH, FSH and oestrogen to decrease

Seen in Anorexia, nutritional deficiencies and strenuous excercise or emotional stress

  1. PCOS
  2. Hyperprolactinemia which inhibits GnRH production.
  3. Hypothyroidism: low thyroid hormone levels causes more TRH to be secreted ->stimulates prolactin release
  4. Premature ovarian failure
  5. Intrauterine Adhesions (Asherman syndrome)
310
Q

What is premature ovarian failure

A

Ovarian Follicles -> undergo accelerated atresia -> depletes before 40 -> Early menopause -> decreased oestrogen and raised FSH and LH

311
Q

What is Asherman Syndrome

A
  1. Intrauterine Adhesions: Scar tissue in uterine cavity in females undergone uterine instrumentation. Causes no functional endometrium left

So endometrium becomes refractory to hormones

312
Q

Symptoms of Turner’s

A
  1. Short stature
  2. Absent Secondary Sex Characteristics
  3. Wide or Webbed Neck
  4. PRIMARY Ammenorheoa
  5. Broad chest with widely spaced nipples
  6. Cubitus Valgus

This is because the X chromsome carries genes for growth and developement: Single copy of SHOX gene (short stature homeobox) causes short stature.

CV defects (coarctation and biscupid aortic valve):

Symptoms of syanosis of lower extrmeities

Horshoe kidneys (they become fused during development)

Symptoms: UTI

Risk for T2DM and hypothyroidism.

These risks get greater depending on how severe genetic is missing

Babies born with lymphedema and lymph related swelling at back of neck (CYSTIC HYGROMA - neck webbing)

313
Q

Symptoms of Mullerian Agenesis

A
  1. Dyspareeunia and infertility

2. Primary amenorrheoa

314
Q

Symptoms of Kallman

A
  1. Absence of smell
315
Q

Symptoms of Functional Hypothalamic Amenorrhoea

A

Decreased wight, bone density and fractures

316
Q

Diagnosis for:

  1. Turner’s
  2. Androgen insensitivity
  3. Mullerian Agenesis
  4. Inauterine adhesions
A

1+2: Karyotyping
2+3: Ultrasound
4: Hysteroscopy

317
Q

Treatment of turner’s, pcos, premature ovarian failure

A
  1. Hormone Replacement Therapy (OCOP)
318
Q

Treatment of prolactinoma

A

Cabergoline which inhibits prolactin

319
Q

How does the X Karyotype in Turner’s arise (from meiosis)

A

Non Disjunction of chromsoomes (the split is uneven)

Mosaicism

Deleting short-arm but the rest of the chromosome stays in tact - again mosaicism and happens at random.

320
Q

What is mosaicism

A
  1. Follows conception
    Individual has some cells with 45X and 46XX

Non disjunction occurs in subsequent mitosis of the zygote

321
Q

What is cubitus valgus

A

Arms overturned outwards

322
Q

What is Amenorrhoea

A

No menstruation

323
Q

What is primary amenorrhoea

A
  1. Menstruation never starts
324
Q

Three cases in where amenorrheoa is normal

A
  1. Before Puberty
  2. During pregnancy and lactation
  3. After menopause
325
Q

What is the follicular phase

A
  1. Where follicles ‘race’ to become the more dominant mollicule to be released at ovulation
  2. All release oestrogen which suprsses GnRH to rduce FSH and LH production.
326
Q

How long does the menstrual phase last

A

5 Days

327
Q

What is the profilerative phase

A

Follows the menstrual phase where increased in ovarian oestrogen to thicken endometrium layer.

Increased blood supply from spiral artieries to endometrium.

328
Q

What occurs in the luteal phase

A

Occurs after ovulation: where coprus luteum produces progesterone to thicken endometrium:

Spiral arteries continue to grow

If not fertilised: Progesterone and oestrogen levels decrease

329
Q

When are people diagnsoed with Amenorrheoa

A

After age 16 (suspected after 13 with no menarche)

330
Q

Most common cause of primary amenorrheoa

A

Turner Syndrome (45, X) - where one chromosome is completely absent They have 45 instead of 46 chromosomes

secondary cause: Müllerian Agenesis (MRKH syndrome)

Rare: ANdrogen Insensitivity Syndrome and Kallman syndrome

331
Q

What are ovaries replaced by in Turner’s and how is this seen on histology

A
  1. Streak Gonads (functional, fibrous tissues)

Turner’s causes accelerated degeneration of ovarian follicles - menopause before menarche

No Ovarian oestrogen means less inhibition on GnRH = raised LH and FSH

332
Q

What is MRKH syndrome

A

Mullerian ducts responsible for Uterus, cervix, upper 2/3rds vagina do not develop. and are thus, absent or obstructed: absence of menses.

Ovaries develop normally and produces oestrogen so FSH and LH are normal.

333
Q

What is androgen insensitivity syndrome

A

Biologically male (46, XY) but tissues do not respond to testosterone.

No uterus, fallopian tubes or ovaries - menses absent

Have testicales stuck in the ignuinal canal or abdomen which produce testosterone (keeping LH and FSH normal)

334
Q

Consequence of testosterone production by testicles that isn’t binding to tissues in AIS

A
  1. Excess -> converted to oestrogen causing development of female secondary sex characteristics.
335
Q

What is Kallman syndrome

A

Neurons failt o migrate from nose to hypothalamus during fetal development: low levels of GnRH, FSH and LH -> low oestrogen

So puberty never starts or is incomplete.

336
Q

What is secondary amenorrhoea

A

At least 3 menstrual cycles for women who had regular cycles, 6 months for females who had irregular cycles.

337
Q

Most common causes of secondary amenorrheoa

A
  1. Pregnancy
  2. Functional Hypothalamic amenorrheoa - where decreased GnRH secretion causes LH, FSH and oestrogen to decrease

Seen in Anorexia, nutritional deficiencies and strenuous excercise or emotional stress

  1. PCOS
  2. Hyperprolactinemia which inhibits GnRH production.
  3. Hypothyroidism: low thyroid hormone levels causes more TRH to be secreted ->stimulates prolactin release
  4. Premature ovarian failure
  5. Intrauterine Adhesions (Asherman syndrome)
338
Q

What is premature ovarian failure

A

Ovarian Follicles -> undergo accelerated atresia -> depletes before 40 -> Early menopause -> decreased oestrogen and raised FSH and LH

339
Q

What is Asherman Syndrome

A
  1. Intrauterine Adhesions: Scar tissue in uterine cavity in females undergone uterine instrumentation. Causes no functional endometrium left. Collagen -> adhesions

So endometrium becomes refractory to hormones

Olfactor placode contains olfactor neurons which migrate to cribriform plate and have neurones secreting GnRH which pass thorugh cribriform plate and settle in the pituitary glands

340
Q

Symptoms of Turner’s

A
  1. Short stature
  2. Absent Secondary Sex Characteristics
  3. Wide or Webbed Neck
  4. PRIMARY Ammenorheoa
  5. Broad chest with widely spaced nipples
  6. Cubitus Valgus

This is because the X chromsome carries genes for growth and developement: Single copy of SHOX gene (short stature homeobox) causes short stature.

CV defects (coarctation and biscupid aortic valve):

Symptoms of syanosis of lower extrmeities

Horshoe kidneys (they become fused during development)

Symptoms: UTI

Risk for T2DM and hypothyroidism.

These risks get greater depending on how severe genetic is missing

Babies born with lymphedema and lymph related swelling at back of neck (CYSTIC HYGROMA - neck webbing)

341
Q

Symptoms of Mullerian Agenesis

A
  1. Dyspareeunia and infertility

2. Primary amenorrheoa

342
Q

Symptoms of Kallman

A
  1. Absence of smell (hyposmia or anosmia)

Low GnRH means

REDUCED Testosterone in men

REDUCED progesterone and oestrogen in women

Stops puberty from happening

It’s a HYPOgonadotropic HYPOgonadism disorder

343
Q

Symptoms of Functional Hypothalamic Amenorrhoea

A

Decreased wight, bone density and fractures

344
Q

Diagnosis for:

  1. Turner’s
  2. Androgen insensitivity
  3. Mullerian Agenesis
  4. Inauterine adhesions
A

1+2: Karyotyping
2+3: Ultrasound
4: Hysteroscopy

345
Q

Treatment of turner’s, pcos, premature ovarian failure

A
  1. Hormone Replacement Therapy (OCOP)
346
Q

Treatment of prolactinoma

A

Cabergoline which inhibits prolactin

347
Q

How does the X Karyotype in Turner’s arise (from meiosis)

A

Non Disjunction of chromsoomes (the split is uneven)

Mosaicism

Deleting short-arm but the rest of the chromosome stays in tact - again mosaicism and happens at random.

348
Q

What is mosaicism

A
  1. Follows conception
    Individual has some cells with 45X and 46XX

Non disjunction occurs in subsequent mitosis of the zygote

349
Q

What is cubitus valgus

A

Arms overturned outwards

350
Q

Where is GnRH released

A

Hypophyseal portal system

351
Q

WHat cells are responsible for the production of sperm

A

Sertoli Cells - FSH

352
Q

What cell does LH bind to in women

A

Theca cells - produce andostendione and progestrone

353
Q

What cells covert androstendione to oestrogen

A

Granulosa cells

354
Q

Male-specific symptoms in Kallman syndrome

A
  1. Small penis and testes
  2. Improper testicular decent
  3. Low SPERM count

Low muscle mass, deep voice or facial hair

355
Q

Women-specific symptoms in Kallman syndrome

A
  1. Amenorrheoa
  2. Oligomenorrhoea
  3. Lack of breast and pubic hair development

INFERTILITY

Osteoporosis in both genders

356
Q

What causes endometritis

A
  1. Normal Bacterial Flora of lower genital tract

USUALLY caused by retention of products of conception (placental or fetal tissue after delivery or abortion)

IAU, contraception

Bactera: C. trachomatis, n.gonnorhoea, M tuberculosis which can travel down

357
Q

Symptoms of acute endometritis

A
  1. Fever
  2. Abnormal uterine bleeding
  3. Lower abdo pain
  4. Dysuria
  5. Dyspareunia
358
Q

Symptoms of chornic endometritis

A

Normal, maybe some pain

359
Q

Diagonosis of endometritis

A
  1. Microsopcic: Neutrophils in endometrium - ACUTE
  2. Lymphocytes in endometrium - CHRONIC
  3. Chronic granulomatous endomtritis (granulomas) - TB
360
Q

What causes endometrial hyperplasia

A
  1. Long standing exposure to high oestrogen levels with no counteracting progesterone
361
Q

RF for endometrial hyperplasia

A
  1. Obesity (extra adipose converts androgen to oestrogen)
  2. Tumours secreting oestrogen (granulosa cell tumours of ovaries)
  3. PCOS (follicles all secrete oestrogen so no luteal body to secrete progesterone)
  4. NUMBER OF YEARS EXPOSED TO OESTROGEN so early menarche, late menopause, nulliparous (no pregnant women)
362
Q

Why are pregannt women less likely to hav eendometrial hyperplasia

A
  1. Because more oestorgen and progestrone is produced, then more progesterone is produced which is protective
363
Q

What drugs can cause endometrial hyperplasia

A
  1. Oestrogen HRT

2. Tamoxifen (breast cancer medication that blocks oestrogen receptors but stimulates endometrium)

364
Q

Risk factor for endometrial cancer

A

Hyperplasia - dpeends on the histological features of hyperplasia

  1. Age; 55-65
  2. FH of Hereditary nonpolyposis colorectal cancer (lynch syndrome)
365
Q

Types of histoological appearances for endometrial hyperplasia

A
  1. Simple: Ratio of dilated glands to stroma is similar to normal tissues
  2. Complex: More glands and less stroma (high ratio) - more at risk of cancer
366
Q

Main type of endometrial carcinoma

A
  1. Endometriod carcinoma (TYPE 1)

Where the cancer cell looks like normal endometrial cells

Linked to hyperplasia (prolongued expsure)

  1. Less common is Type 2
367
Q

What genetic mutation is involved in endometrioid carcinoma

A
  1. Loss of PTEN tumour supressor gene
368
Q

Sub-types of type 2 (not linked to oestrogen) endometrial cancer

A
  1. Serous carcnioma
369
Q

Histology of serous carcinoma

A
  1. Psammoma bodies (finger like calcium deposits around necrotic cells)
370
Q

RF for type 2 endometrial cancer

A
  1. Endometrial atrophy (more aggressive) and happen in older women
371
Q

gene foundin type 2 denometrial cancer

A

TP53

372
Q

Symptoms of Endomterial hyperplasia and carcinoma

A
  1. Menorrhagia (heavy)
  2. Metorrhagia (between cycles)
  3. Menometrorrhagia (combination of both)

ANY painless vaginal bleeding in postmenopausal women (suspect hypeprlasia or cancer)

  1. Enlargement of WHOLE uterus is bound to cause abdo pain and cramping.
373
Q

Diagnosis of hyperplasia and carcinoma

A

Transvaginal ultrasound and biopsy to confirm

374
Q

Treatment of hyperplasia

A
  1. Stopping drugs
  2. Weight loss
  3. Correcting anovulation
  4. Progesterone medications

Cancer is treated by hysterectomy with bilateral salpingo-oophorectomy

Removal of pelvic and para-aortic lymph notes

Raido and chemotherapy

375
Q

What are endometrial polups

A
  1. Benign growth of the endometrium layers
376
Q

RF for endometrial polyps

A
  1. Frequent Tamoxifen therapy

HISTORY of breast cancer treatment

377
Q

Symptoms of endometrial polyps

A
  1. Asymptomatic
  2. Abnormal uterine bleeding

Diagnosed with TVUSS

378
Q

What is Adenomyosis

A
  1. Endometrial tissue develops ectopically in myometrium

This then repsonds to hormonal changes

379
Q

Symptoms of adenomyosis

A
  1. Dysmenorrhoea
  2. Heavy menstrual bleeding
  3. chronic pain
380
Q

Physical exam founding of adenomyosis

A
  1. Enlarged, globular and boggy soft on palpation
381
Q

Diagnosis of adenomyosis

A
  1. Histopathological analysis of uterus after hysterectomy

If they wish to have children, just symptom relief using OCOP GnRH modulators.

382
Q

What are leiomyomas

A

Uterine fibroids - bengin tumours of smooth muscle.

383
Q

How are leiomyomas classified

A
  1. Based on location:

Intramural (develop in uterine wall)

Submucosal fibroids (smooth muscle cells from endometrium)

Subserosal fibroids (smooh cells at perimetrium)

Pedunculated (if they grow into uterus cavity)

Usually develop in groups

384
Q

RF of uterine fibroids

A
  1. African decent
  2. More oestrogen = more fibroids so age: 2040 and pregnancy
  3. Nulliparous
  4. Early menarche
  5. Late menopause
385
Q

Symptoms of leiomyomas

A
  1. Abnormal uterine bleeding
  2. Abdo pain
  3. Fullness feeling
  4. Iron deficiency anaemia in premenopausal women

Submucousal and intramural: Infertility and miscarriage

Pregnancy:
Preterm labour
Postpartum haemorrhage
Fetal malpresentation

386
Q

Diagnosis of uterine fibroids

A
  1. Pelvic exam followed by USS

3. Biopsy

387
Q

Gross examination of fibroids

A
  1. Round, firm and grayish-white

2. Necrosis or haemorrhage

388
Q

Microsocpic exam of fibroids

A
  1. Whorled-pattern of smooth muscle (wave-like)
389
Q

Treatment of symptomatic fibroids

A
  1. Myomectomy/hysterectomy/uterine artery embolization using a catheter
390
Q

What is leiomyoscaroma

A

Rare smooth muscle from myometrium

DE NOVO (they do not progress, they start as a sarcoma)

391
Q

RF of leiomyosarcoma

A

Postmenopausal individuals

392
Q

Symptoms of leiomyosarcoma

A
  1. Abnormal uterine bleeding

2. Abdominal pelvic pain or pressure.

393
Q

Diagnosis of leiomyosarcoma

A
  1. Ultra sound
  2. Biopsy

Leiomyomas have no necrosis or haemorrhage while leiomyosarcoma have a single lesion and necrosis/haemorrhage

394
Q

Name the two layers of the cervix

A
  1. Endocervix (columnar epithelial cells)
  2. Ectocervix (mature squamousepithelial cells)

Meet at the squamocolumnar junction. This has the transofmration zone where immature cells multiply and differentiate.

395
Q

What is metaplasia

A

Where stem cells differentiate to a cell type that replaces the normal specialised cells in a tissue (replacable)

396
Q

What is dysplasia

A

Fully diffrentiated cells regress into immature cells (varying)

397
Q

Where does cervical intraepithelial neoplasia take place

A

In the basal layer of the transformation zone - dysplasia

398
Q

What causes cervical intraepithelial neoplasia

A

HPV infection (16,18,31,33)

These invade stratified epithelial cells (immature where high cell turnover because of rubbing together of surfaces - anus)

6 and 11 are low risk and cause warts

399
Q

High risk HPV strains vs low risk

A

High risk makes huge amounts of E6 and E7 proteins using host DNA which push mature squamous cells through cell replication by blocking tumour suppression genes.

Leads to uncontrolled replication.

400
Q

RF for HPV

A
  1. Multiple sexual partners
  2. Not using condoms
  3. Smoking
  4. Immunosuppression
  5. Early age at first sexual intercourse
401
Q

What are koilocytes

A

Dysplastic, HPV infected epithelial cells

These cells accumulate in cervical epithelium from basal layer onwards.

402
Q

Histological characteristics of koilocytes

A
  1. Immature squamous
  2. Dense, irregular staining
  3. Perinuclear clearing (halo)
403
Q

Grading of cervical intraepithelial neoplasia

A
  1. CIN 1 (1/3rd basal layer)
  2. CIN 2 (affects 2/3rds)
  3. CIN 3 (Almost All epithelium)
  4. CIS (in situ) entire thickness affected.

After CIS, cancerous cells break through epithelial basement membrane and cervical stroma.

Squamous cell carcnioma

The higher the grade, the more likely progression to carcnioma.

Progression fro infection to CIN to cancer is slow (can take between 10-30 years typically presents between 40-50)

404
Q

What is the second most common type of cervical cancer

A

Adenocarcnioma arising from epithelial gland cells of cervix.

Associated with HPV.

405
Q

Symptoms of cervical cancer

A
  1. Spreads to nearing tissues like uterus and vagina- thus metastatic from cervix and can even invade through periteal cavity to abdomen and anus.
  2. If it invades and blocks ureters, can cause hydronephrosis -> renal failure. As kidneys produce urine but cannot drain so causes distention of renal pelvis and kidneys.

Causes flank pain

  1. Spread through lymphatic systems to lungs and liver.

Causes pelvic pain

  1. Spread to bladder:
    - Urinary frequency
    - Dysuria
    - Haematuria
  2. Rectum:
    Constipation

Asymptomatic for a long time:

  1. Postcoital bleeding
  2. Vaginal discomfort
  3. Foul smelling vaginal discharge
406
Q

How is screening for CIN and cervical cancer done

A
  1. PAP smear to test for dysplasia (pos or neg). If pos, then colposcopy is done to obtain biopsy.
  2. HPV DNA testing to see if its high risk
  3. WORLDWIDE cervical cancer most common gyne cancer
407
Q

How is CIN and cervical cancer diagnosed

A
  1. Pelvic exam for lesionss (looks like an ulceration) + barrel shaped cervix where mass is enlarged, indurated.
  2. Confirmed by biopsy and MRI for metastasis.
408
Q

How is CIN treated

A
  1. Local excision by cryosurgery or Conization
409
Q

What is conization

A

Removal of transformation zone.

410
Q

How is cervical cancer treated

A
  1. Tumour removal or uterus and lymph nodes.
411
Q

What strains does the HPV vaccine protect against

A 
1. 16
18
31
33
45
52
58

6,11

412
Q

What is Rokitansky protuberance

A

When hair, dermal appendages, bone and teeth are present, projecting from the white shiny Masses from the wall of a cystic teratoma towards the centre of the cyst.

413
Q

What is the management steps for a negative hrHPV

A
  1. Return to normal recall
414
Q

4 Exceptions to a negative hrHPV test

A
  1. test of cure pathway: individuals treated for CIN1, CIN2, or CIN3 should be invited 6 months after treatment for a test of cure
  2. Untreated CIN1 pathway
  3. Follow up for incompletely excised CIN
  4. Follow up borderline changes in endocervical cells
415
Q

What are the management steps for a positive hrHPV

A
  1. Cytological examination of samples

2. Colposcopy to check for dyskaryosib , invasive cell carcinoma or glandular neoplasia

416
Q

If cytology is normal following a positive hrHPV test, what is done

A

Repeat test in 12 months . I fnevative again, return to normal recall, if positive = repeat again in 12 months

417
Q

If hrHPV remains +ve at 24 months, what should be done

A

Colposcopy

418
Q

If a hrHPV sample is deemed inadequate, what should be done

A

Repeat sample within 3 months

419
Q

What is premenstrual syndrome

A

Emotional and physical symptoms women may experience during the luteal phase of the normal mestrual cycle (e.g., anxiety, stress, fatigue and mood swings) or breast pain and bloating

420
Q

Management of PNS

A
  1. regular, frequent (2-3 hourly) small balanced meals rich in complex carbs
  2. COCP
  3. SSRIs for severe symptoms for mood.
421
Q

Classic symptom of endometrial cancer

A

Postmenopausal bleeding

2. Premenopausal women may have changes in intermenstrual bleeding

422
Q

Classic sign of endometriosis

A
  1. Long history of pelvic pain, that increases in severity during menstruation. Pain reduces in the absence of mesntruation
423
Q

What is PID

A

Infection and inflammation of the female pelvic organs such as the uterus, Fallopian tubes and surrounding peritoneum. Acending infections from c trachmatis, gonorrhoea and mycoplasma

424
Q

Treatment of PID

A
  1. Oral oflaxacin + metronidazole
425
Q

Complications of PID

A
  1. Fitz-Hugh Curtis Syndrome (RUQ pain) - peri hepatitis
  2. Ectopic pregnancy
  3. Infetility
426
Q

How long can a urine pregnancy test stay positive for after termination

A

4 weeks

427
Q

What is the trend in hCG levels following termination

A

Initial steep decline in first two weeks followed by gradual decline over a further two weeks

428
Q

Who is needed to approve a pregnancy

A

Two medical practitioners in a listened NHS hospital

429
Q

What is the upper limit for an abortion

A

24 weeks

430
Q

What is the method used to terminate a pregnancy at 9 week gestation

A

Mifepristone followed by vaginal misoprostol to stimulate uterine contractions

431
Q

When should individuals treated for CINI, 2 or 3 be invited for a follow up

A

6 months

432
Q

What treatment should be given to pregnant women who have thrush

A

Clotrimazole pessary as fluconazole is contraindicated.

433
Q

What is the only effective treatment for large fibroids causing fertility problems

A

Myomectomy

434
Q

What is stress incontinence

A

The weakening or damage to the muscles preventing urination

435
Q

What is urge incontinence

A

Overactivity of the detrusor muscles

436
Q

How is urge incontinence treated

A

Bladder retraining

437
Q

How is stress incontinence treated

A

Pelvic floor muscle training or Duloxetine

438
Q

What is the GOLD STANDARD for endometriosis

A

Laparoscopy

439
Q

Investigations for ovarian cancer

A

CA125

2. TVUSS

440
Q

On examination, what is characteristic of endometriosis

A

A fixed, retroverted uterus.

441
Q

What is the main form of vulval cancer

A

Squamous cell carcinoma

442
Q

RF for vulval squamous cell carcnioma

A 
over 65
HPV
VIN
Immunosuppression
Lichen Sclerosus
443
Q

Features of vulval carcnioma

A
  1. Lump or ulcer on labia majora
  2. Inguinal lymphadenopathy
  3. Itching and irritation
444
Q

What is Meigs’s syndrome

A
  1. Triad of ascites, pleural effusion and banging. ovarian tumours. effusion Classically on the right
445
Q

What is Meigs’s syndrome typically associated with

A
  1. Fibromas
446
Q

Most common cause of ovarian enlargement in women of a reproductive age

A

Follicular cyst

447
Q

Most common benign ovarian tumour in women under the age of 25

A

Teratoma

448
Q

What causes a corpus lute cyst

A

If the pregnancy doesn’t occur, the corpus lute should break down, if this doesn’t happen it forms a cyst

449
Q

Serous vs mutinous cystasenomas

A

Arise from the ovarian surface epithelium

Bears resemblance to serous carcinoma vs can cause pseudomyxoma peritonea.

450
Q

Examination findings in a complete miscarriage vs a missed miscarriage

A
  1. Empty uterus of TVUSS with heavy blood loss vs a feotus with no cardiac activity.
451
Q

What system is used to score the severity of nausea and vomiting in pregnancies

A
  1. Pregnancy-Unique Qualification of Emesis.
452
Q

RF for cervical ectropion

A

COCP, due to higher oestrogen level.s

453
Q

When is a laparoscopic salpingectomy indicated for an ectopic pregnancy

A

> 35mm in size.

454
Q

Long term complications of a vaginal hysterectomy with anteroom-posterior repair

A

Enterocele

Vaginal vault prolapse

455
Q

In what condition is a strawberry cervix (erythematous cervix with pinpoint areas of exudation) found

A

Trichomonas vaginalis.

456
Q

How is stage 1 of endometrial cancer treated

A

Hysterectomy with bilateral salpingo-oophorectomy

457
Q

Fibroids vs adenomyoisis

A

Uterus feels bulky on examination vs boggy uterus with subendometrial linear striations.

458
Q

What is an ovulation test

A

Day 21 progesterone levels

459
Q

When is a day 21 progesterone test indicated

A

If a woman of a reproductive age has not conceived after 1 year of unprotected vaginal sexual intercourse with no known cause for infertility.

460
Q

Symptoms of urogenital prolapse

A

Seen in ODLER WOMEN:

Sensation of pressure, heaviness or ‘bearing down’.

461
Q

What ca reduce the risk of endometrial hyperplasia and carcnioma in people with PCOS

A

Levonorgestrel-releasing intrauterine system.

462
Q

What is Mittelschmerz

A
  1. Occurs due to the small amount of fluid released during ovulation. Pain settles between 24-48 hours.
463
Q

Most common complication of pregnancy termination (including when given misoprostal and mifepristone)

A

Infection.

464
Q

What is ovarian hyper stimulation syndrome

A

Seen in infertility treatments

  1. Often result in multiple luteinized cysts causing VEGF and other vasoactive substances to surge. Causes increased membrane permeability and loss of fluid.
465
Q

Symptoms of ovarian hyper stimulation syndrome

A

Mild: Abdo Pain
Abdo bleeding

Modderate: Nausea and vomiting
Ascites

Severe: Ascites
Oliguria
Haematocrit > 45%

Hypoproteinaemia

Critical: ARDS
Anuria
Tense Ascites

466
Q

When should Semen Analysis be performed (how long should they abstain)

A

Between 3 to 5 days

467
Q

When should a semen test be repeated

A

If there is mild oligozoospermia, repeat test in 3 months.

468
Q

What would be seen in PID during a hysterosaplingography

A

Bilateral blocked Fallopian tubes

469
Q

What is the classic triad for IBS

A

Abdominal Pain
Bloating
Change in Bowel Habit

470
Q

What is fibroid degeneration

A
  1. Uterine fibroids are sensitive to oestrogen and grow during pregnancy. If they outstrip their blood supply, they go degeneration, where they present with pain, fever and committing.
471
Q

Management of fibroid degeneration

A

Rest and analgesia.

472
Q

Role of tranexamic acid

A

Used to treat or prevent excessive blood loss, and often used in emergencies.

473
Q

When do fibroids begin to regress

A

Following menopause

474
Q

What is the criteria of expectant management for an ectopic pregnancy (watchful waiting)

A
  1. An enraptured embryo
  2. <35mm in size
  3. No Heartbeat
  4. Be asymptomatic
  5. Have a B-hCG level of <1,0000 IU/L and declining.
475
Q

When is surgical management of an ectopic pregnancy needed

A
  1. Sizer >35mm
  2. Rupturable/signs of infection
  3. Pain
  4. Visible foetal heartbeat
  5. Serum B-hCG > 1,5000 IU/L
476
Q

What is medical management of an ectopic pregnancy

A

Methotrexate

477
Q

What level of serum progesterone indicates ovulation

A

> 30 nmol/L

478
Q

Three components of the Risk Malignancy Index for Ovarian Cancer

A
  1. USS findings
  2. Menopausal status
  3. CA125
479
Q

What is a vesicovaginal fistula

A

An opening between the bladder and the vagina

480
Q

Symptoms of vesicovaginal fistulas

A

Continous dribbling incontinence after prolonged labour

481
Q

What causes overflow incontinence

A

Bladder Outlet Obstruction (e.g., protostar enlargement)

482
Q

Examination for Incontninecen

A
  1. Bladder diaries for 3 days

2. Urodynamic studies

483
Q

What is the routine cervical smear call for:

  • 25-49
  • 50-65
A

25-49: Every 3 years

50-65: Every 5 years

484
Q

What defines menopause

A

Amenorrhoea for > 1 year

485
Q

When should a cyclical HRT regime be used over continuous

A

When a patient has not yet achieved her menopause (perimenopausal)

486
Q

What is cyclical combined HRT

A

Oestrogen is given daily, but progesterone is only used for a few weeks in the cycle.

487
Q

What is a contraindication for HRT

A

Undiagnosed vaginal bleeding
Current or past breast cancer
Untreated endometrial hyperplasia

488
Q

How long do menopausal symptoms last for

A

7 years

489
Q

How are vasomotor symptoms of menopause treated

A

Fluoxetine

490
Q

How long should HRT be used before stopping

A

2-5 years.

491
Q

Treatment for Primary dysmenorrhoea (period pains)

A

NSAIDs (mefanemic acid)

492
Q

Pharmacology of mefanemic acid

A

inhibits both COX-1 and COX-2 , stopping the formation of prostaglandins.

493
Q

Investigations for an ectopic pregnancy

A

TVUSS

494
Q

What investigation is needed to diagnose premature ovarian failure

A

FSH levels (RAISED in menopausal women)

495
Q

What part of the reproductive system, is an ectopic pregnancy most prone to rupture

A

Isthmus

496
Q

Management of women with secondary dysmenorrheoa

A

Refer to gynaecology

497
Q

What condition are dysgermbnomas’s associated with

A

Turner’s

498
Q

What do dysgerminoma’s secrete

A

hCG and LDH

499
Q

What do yolk sac tumours (endodermal sinus tumours) secrete

A

AFP

500
Q

Where do choriocarcinoma’s typically spread

A

To the lungs.

501
Q

What do sertoli-leydig tumours secrete

A

Androgens

502
Q

When do fibromas’s occur

A

Menopause

503
Q

Symptoms of fibroma’s

A

Pulling sensation in the pelvis

504
Q

How is a cervical IA tumour treated

A

Either hysterectomy with node clearance or for maintaining fertility, a c one biopsy with negative margins

505
Q

Management of cervical stage IB tumours

A

Radiotherapy (brachytherapy or external beam radiotherapy) with chemotherapy (cisplatin)

506
Q

How are stage II, III and IV tumours treated

A

Radiation with concurrent chemotherapy

507
Q

Complications of radiotherapy

A

Ovarian failure
Bowel fiborsis
Lymphodemoa

508
Q

Complications of a hysterectomy

A

Urethral fistula

509
Q

In what condition is a whirl pool sign seen

A

Ovarian torsion (bowel twists around itself)

510
Q

First line treatment for menorrhagia (heavy vaginal bleeding)

A

Mirena inauteirine system,

511
Q

When does endometriosis begin to disspitate

A

After menopause as oestrogen levels decline.

512
Q

Management of endometriosis

A

COCP

If wanting to conceive, referral to fertility services.

513
Q

What surgery would improve fertility in women with endometriosis

A

Laporoscopic adhesiolysis.

514
Q

Surgical first line intervention for ectopic pregnancy

A

Salpingectomy.

515
Q

Stages of ovarian cancer metastases

A
  1. Stage 1: confined to ovaries
    Stage 2: Outside ovaries but within the pelvis
    Stage 3: Outside pelvis but within abdomen

Stage 4: Distant Metastasis

516
Q

Symptoms of a ruptured cyst vs ruptured ectopic pregnancy

A

Rupture is caused by intercourse or strenuous activity and has free fluid in pelvic cavity vs rupture for ectopic is unprecedented

517
Q

What drug is given to reduce the size of the fibroid and uterus

A

GnRH agonist (Leuprolide)

518
Q

Why is GnRH given before fibroid surgery

A

To reduce operative blood loss

519
Q

Symptoms of APS

A
  1. Low platelet count
  2. Livedo reticulais
  3. Dementia/headaches
520
Q

Genetic markers for APS

A

HLA-DR4, HLA-DR7

521
Q

Autoimmune proteins in APS

A
  1. Anti-cardiolipin antibodies (inhibits protein C)
  2. Lupus anticoagulant antibodies (bind to prothrombin, increasing cleavage to thrombin)
  3. Anti-ApoH.
522
Q

Consequences of APS

A

Recurrent miscarriage
2. Inauterine growth restriction
Preterm birth

523
Q

How long do post-menopausal women have to wear contraception for (over 50)

A

2 years after last menstrual period (1 for people over 50)

524
Q

What is vaginal vault prolapse

A
  1. When the top of the vagina slips from its normal position and sags down
525
Q

What usually causes a vaginal vault prolapse

A

Hysterectomy

526
Q

Surgical treatment of vaginal vault prolapse

A

Sacrocolpopexy

527
Q

What is the secrocolpopexy

A

Suspends the vaginal apex to sacral promontory

528
Q

What is a cystocele

A

When the wall between the bladder and th evagina weekends, causing the bladder to drop or sag into the vagina

529
Q

RF for cystocele

A

Age
Overweight
Child birth
Heavy lifting

530
Q

Symptoms of a cystocele

A

Pelvic heaviness or fullness
Lower back pain
UTIs
Urinary urgency, frequency, hesitancy, poor flow, post micturition dribbling and feeling of an incomplete bladder.

531
Q

Surgical treatment of a cystocele

A

Anterior colporrhaphy

532
Q

Management of a cystocele

A

Keagel’s

533
Q

Surgical intervention of a uterine prolapse

A

Hysterectomy

534
Q

Surgical intervention of a rectocele

A

Posterior colporrhaphy

535
Q

What gynaecological condition can cause Wernicke’s encephalopathy

A

Hyperemesis Gravidarum

536
Q

When should progesterone levels be checked when checking for subferitlity

A

Day 21 OR 7 days before the end of the cycle.

537
Q

Most common type of epithelial cell tumour

A

Serous cyst adenoma

538
Q

Most common form of secondary amenorrhoea in a very athletic woman and why

A

Hypothalamic hypogonadism:

Because in women with low fat levels, the hypothalamus releases less GnRH = hypogonadism

Less successful pregnancies!

539
Q

What criteria is used to diagnose PCOS

A

Rotterdamn criteria

540
Q

What is the Rotterdam criteria

A

Anovulation and Hyperandrogenism

541
Q

How should a HIV patient be screening for CIN

A

Annual cervical cytology.

542
Q

Describe the RAAS system

A

The juxtaglomurelar cells contain Baroreceptors to detect low BP

  1. High BP: Inhibit Renin release
  2. Low BP: Stimulate Renin release
  3. Information travels to mechanoreceptors via the sympathetic nerve fibres at the carotid sinus and aortic arch.
  4. Macula Densa Cells detect GFR: When BP rises, GFR rises. More fluid and Na+ and Cl- reach macula densa. which is sent back to the baroreceptors of the juxtaglomerular cells
  5. Renin -> plasma -> angiotensinogen -> cleaves -> angiotensin I -> flots to the livers -> endothelial cell ACE cleaves 2 amino acids -> angiotensin II

Angiotensin II binds to receptors, causing smooth muscle contraction. and aldosterone secretion

Causes efferent arterioles to constrict or dilate.

543
Q

What is produced in the zone resticularis

A

DHEA and Androstenedione

544
Q

What is produced in the zone fascilculata

A

Glucocorticoids (cortisol)

545
Q

What is produced in the zone glomerulosa

A

Mineralocorticoids (aldosterone)

546
Q

Role of aldosterone

A

Binds to DCT cells, Na+/K+ move K+ from blood into the urine and Na+ from tubules into blood. Water moves in with Na+ to increase BP

Binds to alpha-intercalated cells ATPase pumps, excreting H+ and moving HCO3- ions into extracellular space = metabolic alkalosis

547
Q

Common source of a krukenberg tumour

A

Gastric adenocarcinomas

548
Q

Management of gender identity crisis

A
  1. Referral to gender identity clinic

2. Referral to local psychiatric services if low mood or deliberate self harm involved

549
Q

How many assessments do a gender identity clinic require

A

Typically 2

550
Q

Cosmetic surgery for a trans male

A

Bilateral mastectomy with male chest reconstruction

551
Q

What two surgeries are conducted for trans male

A

Hysterectomy

Oopherectomy

552
Q

What does the NHS not fund for trans patients

A

ENT, mammoplasty or facial surgery

553
Q

When can cross sex hormones be prescribed

A

16 years old

554
Q

What medications are given to trans women

A 
SC Goserelin (1 or 3 months)
Leuprorelin

Estradiol Valerate
Finasteride
Cyproperone Acetate
Sprinolcatone

555
Q

When are gel and transdermal patches of estradiol particularly indicated

A

Over 40, smokers or chronic disease due to DVT

556
Q

What is Goserelin

A

A GnRH agonist, : increases LH production before sensitising receptors and inhibiting LLH and FSH production: prevents development of secondary sex characteristics.

557
Q

Four effects of feminising hormones

A
  1. Body fat redistribution
  2. Decreased muscle mass
  3. Skin Softening
  4. Decreased libido
  5. Decreased erections
  6. Breast growth
  7. Reduced sperm countr
558
Q

How long does it take for feminising hormones to take effect

A

3-6 months

559
Q

Risks of feminising hormones

A
  1. DVT
  2. Gallstones
  3. Elevated LFTs
  4. Weight Gain
560
Q

How do feminising hormones affect prostate cancer

A

Reduces it

561
Q

When iso estradiol stopped during surgery (trans)

A
  1. 4-6 weeks before. GnRH analogues do not need to be stopped.
562
Q

When can GnRH analogues be stopped

A

After gonadectomy

563
Q

What treatment is lifelong in trans women

A

Oestradiol

564
Q

How often do trans women need to be monitored for

A

6 monthly

565
Q

How long do trans men need testosterone for

A

Life long

566
Q

Why does haematocrit levels need to be monitored in trans men

A

Because adult male RBC mass is greater than in women.

567
Q

How is testosterone given to trans men

A

Testosterone undecanoate (1gm in 4mls every 10-20 weeks)

568
Q

How do topical testosterones need to be taken

A

Serum levels of testoesterone need to be taken 4-6 hours after application

569
Q

If Hb are elevated in trans men, what should be done to the testosterone dose

A

Needs to be reduced

570
Q

How is ovarian suppression done

A

Goserelin implant every 4 weeks and then moved to 12 weeks 10.8mg dose.

571
Q

Side effects of goserelin

A

Hot flushes
Depression
Loss of libido

572
Q

When is goserelin contraindicated in trans men

A

Pregnancy

573
Q

Why is ovarian suppression done

A

To achieve estradiol levels similar to men

574
Q

When in management is ovarian suppression introduced

A

After the introduction of testosterone.

575
Q

4 effects of masculinising hormone therapy

A 
Clitralmegaly 
Body fat redistribution 
Vaginal atrophy 
Cessation of menses
Deep voice
576
Q

Risks of masculinising hormones

A
  1. Polycythaemia (can cause strokes)
  2. Weight Gain
  3. Acne
  4. Androgenic alopecia
577
Q

What is the implication of Oligospermia/ Azoospermia with:

Raised serum FSH and LH

Low Testosterone levels

A

Primary defect in spermatogenesis (hypergonadroptopic hypogonadism)

578
Q

Threshold for oligohydramnios

A

AFI <5

579
Q

Theshold for polyhydramnnios

A

AFI >8

580
Q

Why does hyperemesis gravid arum cause metabolic alkalosis

A

LOSS OF H+,

581
Q

How is metabolic alkalosis corrected

A

Pancrease produces HCO3- but this ends up in the blood not the intestines

582
Q

First line treatment to treat infertility in PCOS

A

Letrozole (not clomiphene citrate)

583
Q

Pharmacology of letrozole

A
  1. Aromatase inhibitor, reduces negative feedback caused by oestrogen, increasing FSH proudction and allowing follicular rupture
584
Q

Treatment of a prolactinoma

A

Bromocriptine

585
Q

Pharmacology of bromocriptine

A

Dopamine receptor agonist

586
Q

What is the first line treatment for obese women with PCOS struggling to conceive

A

Metformin

587
Q

How should hirsutism be managed

A

COCP

588
Q

Treatment of recurrent vaginal candidasis

A

Oral fluconazole (think Tom)

589
Q

What is the action of metformin

A

Increases peripheral insulin sensitivity

590
Q

What family history is a strong precursor for endometrial cancer

A

HNPCCC/ Lynch Syndrome.

591
Q

What other structures may ovarian cysts press against

A

The Bladder (signs of urinary frequency etc)

592
Q

When is referral for facial hair depilation or mastectomy

A

12 months

593
Q

When are hormone therapy started

A

6 months

594
Q

How long does transition tend to take

A

3-5 years

595
Q

Name three anti-androgens

A

Finasteride
Cypropterone
Spironolactone (androgen receptor antagonist)

596
Q

What medication is given to trans men to control mensturtaion

A

GnRH agonist

597
Q

Two forms of testosterone

A

IM injection

Transdermal gel

598
Q

How often are injections monitored for (trans mens hormones)

A

3 months (6-8 weeks for transdermal patches)

599
Q

Continual monitoring for transmen

A

Every 6 months for 3 years

600
Q

Main risk of feminising hormones

A

VTE

601
Q

When are feminising hormones reduced in dose

A

After the age of 50.

602
Q

What is the initial management of a miscarriage

A

Vaginal misoprostol

603
Q

What is th gold standard for diagnosing adenomyosis

A

MRI

604
Q

What is the initial management of a medical abortion

A

Mifepristone and prostaglandins (misoprostol)

605
Q

Is a migraine with aura, a contraindication for HRT

A

No

606
Q

How is HRT given

A

Topical

607
Q

If a patient has a mirena coil, what HRT is given

A

Oestrogen patch as the patient’s mirena coil supplies progesterone.

608
Q

What is the primary treatment for stage2-4 ovarian tumours

A

Surgical excision of tumour

609
Q

Why is a transdermal/topical HRT preferred over Oral

A

Does not increase risk of VTEs

610
Q

How is a pregnant woman under 6 weeks managed if they have vaginal bleeding or cramps

A

Send the patient home and manage expectantly

611
Q

What factor is most associated with a miscarriage

A

Obesity

612
Q

What test is done to check for vesicovaginal fistulae

A

Urinary dye studies

613
Q

In what two conditions is cervical excitation found in

A

PID, Ectopic Pregnancy

614
Q

What is the most common cause of recurrent first trimester miscarriages

A

APL

615
Q

What is the most common cause of postcoital bleeding

A

Cervical ectropion

616
Q

How to treat glandular atrophy of endometriosis

A

Oral Progestagens

Depot Provera or Mirena

617
Q

Adenomyosis vs Endometriosis

A

Endo metriosis is in young and nulliparous women

Adenomyosis happen in older women with multiparty

618
Q

A patient presents with an ovarian mass. Investigations reveal a tumour with cells secreting mucin and peripheral nuclei. What tumour is this

A

This is a Kurkenburg tumour, remember signet ring cells appearance under microscopy.

619
Q

What ratio is found in lab tests, that suggest PCOS

A

Elevated LH:FSH ratio (remember, elevated serum oestrogen will inhibit FSH production)

620
Q

What virus can cause hydros fetalis in the womb

A

Parvovirus 19

(remember: slapped cheek appearance).

621
Q

What is the fried egg appearance of a dysgerminoma

A

Germ cells with clear cytoplasm surrounding a central nucleus.

622
Q

What would be seen on a bimanual examination for chlamidyia

A

Cervical motion tenderness (cervicitis)

More likely to be chlamidyia than gonnorheoa as it’s more prevalent.

623
Q

What genetic mutation causes turner’s syndrome

A

Only one chromosome is functional

624
Q

What is the consequence of prolonged tampons or alien objects in the vagina

A

Toxic Shock Syndrome: Staph Aureus infection that causes diffuse erythema that desquaminates as the patient recovers. Also fever, confusion and abdominal pain.

625
Q

Risk Factors for VTE

A 
T - Trauma or Travel
H - Hospitalisation 
R - Relatives (e.g., V Leiden)
O - Old Age 
M - Malignancy
B - Bone Fractures
O - Obesity and Obstetrics
S - Surgery
I - Immobility 
S - Sickness (e.g., APL, Paroxysmal Nocturnal Haemoglobinuria, Nephrotic Syndrome)
626
Q

What medications can cause folic acid deficiency

A

Phenytoin
methotrexate
Pregnancy
Alcohol Excess

627
Q

First Line Treatment of Candidasis

A

Itraconazole

628
Q

What chronic gynecological problem is associated with Ovarian Hyperstimulation Syndrome

A

PCOS

629
Q

What medication is used to treat endometrial cancers

A

Provera (Medroxyprogesterone) - Slows the growth of malignant cells

630
Q

In what Endometrial cancer stages is a total abdominal hysterectomy with bilateral salpingoopherectomy done

A

Stage I and II

631
Q

How is stage IIB endometrial carcinoma treated

A

Wertheim’s radical hysterectomy (removal of the lymph nodes as well)

632
Q

What is the most common complication of a myomectomy

A

Adhesions

633
Q

Indications for referral to colposcopy in two weeks (emergency)

A

Remember - standard is 6 weeks

Usually 2 weeks if there is high-grade dyskaryosib (moderate or severe) on cytology

634
Q

Indications for 6 week colposcopy reviews

A

Inadequate results
Borderline
Low grade (mild) dyskaryosib

635
Q

Ovarian Cysts vs Fibroids presentation

A

Fibroids develop on the uterus (suprapubic tenderness) while Ovarian cysts are unilateral, flank pain

636
Q

When are medical treatments for menorrhagia contraindicated

A

If the fibroid is over 3cm in size (IUS, tranexamic acid and COCP are all contraindicated)

637
Q

What chronic gynaecological condition is a risk factor for ectopic pregnancy

A

Endometriosis

638
Q

Name the two types of abnormalities that can be found on a Pap smear

A

Atypical Swuamous Cells

Cervical Squamous Intrsepithelial Lesions (CSIL)

639
Q

What is a barrel-shaped cervix

A

In cervical cancer: When the tumour develops under the endocervical canal, looks like a mass on speculum examination

640
Q

What is the difference between stage Ia and stage IB cervical cancer

A

Ia - Can only be seen under a microscope + <5mm

Ib - Seen with the naked eye/ >5mm

641
Q

What is stage 2 cervical cancer (2a and 2b)

A

IIA - Upper 2/3rds of the vagina

IIB - Spread to parametric

642
Q

What is stage 3 cervical cancer (IIIa, IIIb, IIIc)

A

IIIa - Lower 3rd of vagina
IIIb - Pelvic wall and ureters
IIIc - Lymph nodes

643
Q

What is stage four cervical cancer

A

Adjacent organs or Distant organ spread

644
Q

What is diagnostic for chlamidyia and gonorrhoea

A

NAAT using a urine sample

Then a urethral swab for gonorrhoea if NAAT is positive

645
Q

What results indicate a successfully treated SYphilis

A

VDRL negative, TPHA positive

646
Q

What factor determines if someone with PID must come into the hospital

A

a fever > 38 degrees

647
Q

How long must the pain last to diagnose endometriosis

A

Over 6 months

648
Q

What is the second line management if COCP is contraindicated

A

Mirena Coil/progesterones

649
Q

What ethnicity is associated with increased risk of ectopic pregnancies

A

Black Race

650
Q

What are the wolffish ducts

A

Embryonic structures that form the male genitalia (stabilised by testosterone)

651
Q

What is the most common type of ovarian tumour in pre-menopausal women

A

Germ cell ovarian tumour

Epithelial Ovarian Tumour is the most common overall but most commonly arise in postmenopausal women

652
Q

When is a salpingostomy indicated over a salpingectomy

A

Incision into the Fallopian tube to remove the pregnancy

Usually preferred/ first line if there has been damage/surgery/infection to the other tube - to preserve fertility

653
Q

When should PID always be suspected

A

Leucocytosis + Fever

654
Q

What is the first line investigation done for suspected ovarian cancers/cysts

A

Usually a TransABDOMINAL USS in girls who aren’t sexually active

Then a TVUSS in sexually active girls.

655
Q

How does Hereditary haemochromatosis lead to amenorrhoea

A

Iron overload - deposits in the hypothalamus and ovaries.

Accompanied by Joint Pain and LIVER FIBROSIS

656
Q

Name two fertility saving treatments used in Grade IA CIA

A

Cone Biopsy

Radical Trachlectomy (removal of cervix, upper vagina and pelvic lymph nodes)

Followed by cervical cerclage

657
Q

What USS finding points to atrophic vaginitis over endometrial cancer

A

ENDOMETRIAL THINNING - Less than 5/4mm in thickness

658
Q

What is the most likely diagnosis for PV bleeding in post menopausal women

A

Atrophic Vaginitis - most likely diagnosi s

But should be sent for Gynecological assessment to check for endometrial cancer

659
Q

First line management of complex cysts (multiloculated)

A

No matter what the size is, these need a biopsy to exclude malignancy

660
Q

What are the M rules for an ovarian cyst

A 
irregular, solid
Ascites
At least 4 papillary sturctures
Irregular multilocular solid tumour
Very strong blood flow

Any of these, and the cyst would need a biopsy

661
Q

What factor reduces the risk of hyperemesis gravidarum

A

Smoking

662
Q

Why is a beta-HCG test repeated in 48 hours

A

Viable Intrauterine Pregnancy: HcG levels will double

Ectopic: hCG stays the same

Miscarriage: hCG will drop

663
Q

When is surgery indicated for fibroids

A

Over 3 cm

664
Q

When is the mirena coil contraindicated in fibroids

A

If there is too much distortion of the cavity

Otherwise, it’s still first line

665
Q

What is anenterocele

A

Prolapse of the small bowel

666
Q

What is the first line investigation for endometriosis

A

TVUSS

Then lapporoscopy as it can cause bowel perforation for no reason if they do not have endometriosis

667
Q

What feature of an ovarian mass means urgent referral to hospital services

A

Over 50:
Abdo distention
Pelvic Pain
Urinary symptoms

668
Q

Management of Bartholin’s gland

A

Incision and drainage

669
Q

When is oestrogen HRT indicated

A

Hysterectomy (no uterus)

On a progesterone pill

670
Q

What is the first line treatment of vasomotor symptoms of menopause

A

HRT

Then Sertraline (actually second line)

671
Q

How to treat low sex drive n Hot

A

Testosterone alongside HRT

672
Q

Treatment of urogenital atrophy in menopause

A

Vaginal oestrogen with HRT

673
Q

Side effect of HRT

A

Initial irregular bleeding, must take note of this

674
Q

First line investigation in adenomyosis

A

TVUSS

675
Q

Immediate management of a uterine fibroid if a woman is trying to conceieve

A

Transexamic Acid

Mirena coil is not an immediate management

676
Q

Why is Metformin given for PCOS

A
  1. Regulates LH secretion
  2. Reduces gluconeogenesis in the liver (less androgens produced)
  3. Apetite Reduction
  4. Decreases sex-hormone binding globulin in the liver
677
Q

First line treatment of stage IA1

A

Conservative management or cone biopsy

678
Q

Management of Stage IA2-IIA cervical cancer

A

<4cm = radical hysterectomy with lymphadenectomy

> 4cm = Chemoradiation

<2cm and wanting to conceive: Radical Trachlectomy and lymphadenectomy

679
Q

First line management of Stage IIB-IVA:

A

Chemotherapy

680
Q

IF TVUSS for suspected endometriosis is normal, what should be done

A

Laporoscopy

681
Q

What surgical intervention Is used for endometriosis if fertility is not a priority

A

Laporoscopic excision

682
Q

Before laparoscopic excision, what should be given to patients

A

GnRH 3 months before surgery

683
Q

A woman presents with high BMI, hyperpigmentation and thickening of the skin across the back of her neck and in both axilla, what is the most likely diagnosis

A

PCOS! Acanthas Nigrans from insulin resistance

684
Q

What is secondary dysmenorrhoea

A

Defined as painful mensturation secondary to pathology

685
Q

Define primary dysmenorrhoea

A

Painful mensturtaion in the absence of underlying pathology

686
Q

When should 3-monthly cyclical HRT be used compared to 1-monthly

A

3 monthly - irregular periods

1 monthly - regular periods

Perimenopausal women

687
Q

When should we conduct a blood hcg test vs immediate transfer to early pregnancy assessment unit

A

Blood HCg - pregnancy of unknown location

Immediate referral - symptomatic abdominal pain, requiring USS

688
Q

When is an USS contraindicated for extopics

A

Before 5 weeks, an ectopic is known as a PUL and requires b-hcg. A ectopic can’t be seen on the scan before 5 weeks so no point admitting to early pregnancy assessment unit.

Over 5 weeks = assessment in hospital and USS

689
Q

When is expectant management indicated for ectopic pregnancies

A

Clinically stable and pin free

hCG levels < 1,000

690
Q

What is expectant management of an ectopic

A

Repeat hCG on days 2, 4 and 7

To continue expectant management, should only drop by 15%

691
Q

When is methotrexate given for ectopic

A

hCG: 1,000-1,500

Have pain but not significant

692
Q

When should surgery be used as first line treatment for ectopic

A

Unable to return for follow-up

Significant pain

hCG > 5,000

Adnexal mass > 35mm

Visible foetal heartbeat

Anyone with hCG 1,500-5,000 can be offered either depending on their pain and the other factors we’ve discussed

693
Q

When should you offer OGTT to PCOS women

A

Impaired fasting glucose (6.1 to 6.9)

694
Q

Should metformin be offered in primary care for PCOS

A

No

695
Q

What does low sex hormone-binding globulin levels indicate

A

Marker for insulin reisstance

696
Q

What medication can be given to induce a bleed in prolonged amenorrhoea

A

Medroxyprogesterone for 14 days

Then TVUSS

697
Q

First line treatment of acne and hirsutism

A

COCP

698
Q

First line management for cyclical breast pain

A

As the woman to keep a pain diary

Re-assurance, tell to wear bra’s

699
Q

When in PCOS should women be offered OGTT

A
700
Q

First line management of Grade 1, low grade dyskariosis in CIN

A

DO NOT TREAT - Just watchful management and refer for another screen in 12 months time

701
Q

What size endometrium would indicate endometrial hyperplasia and a need for a biopsy

A

> 4mm

702
Q

Expectant management vs Medical Management of an ectopic pregnancy

A

Asymptomatic vs little pain

B-HCG < 1,000 vs B-hCG < 1,500

703
Q

Why is a withdrawal bleed done for women with PCOS

A

Because, intervals >3 months between periods causes endometrial hyperplasia in women with PCOS. Giving medroxyprogesterone or an IUS provides opposing oestrogen to keep the endometrium at its current size

704
Q

Under what size, is a cyst considered simple/non concerning

A

<5cm

705
Q

Indications for an endometrial biopsy at hysteroscopy

A

Persistent intermenstrual bleeding in women aged 45 or older

706
Q

If Clomiphene/Letrozole fail in fertility management for someone with PCOS, what is the second line management

A

Second Line: Ovarian Drilling

Third Line: IVF

707
Q

When should a pelvic ultrasound be used in suspected ovarian cancer

A

Serum CA-125 -> Pelvic USS

Only do a pelvic USS if >35 IU/ml

year 3 (25 decks)

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