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Gynaecology Flashcards

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1
Q

Name types of intersex states

A

CAH, AIS, 5 alpha Reductase

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2
Q

Which intersex state may present later in life?

A

AIS - presents with amenorhoea

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3
Q

What is CAH?

A

Autosomal recessive.
Usually 21 hydroxylase deficiency
Reduction in cortisol and aldosterone
ACTH increases bu shunting into androgen synthesis pathway

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4
Q

What are the symptoms of CAH?

A

Salt wasting
Addisonian crisis in infants
Precocious puberty in males
Virilisation of genitalia in female - ambigous

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5
Q

What are the investigations of CAH?

A

imaging - pelvic/renal/bladder

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6
Q

What is the management of CAH?

A

gender reassignment and replacement of cortisol and aldosterone

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7
Q

What is AIS?

A

High resistance to testosterone causing genetically male children to have a female phenotype

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8
Q

What are the symptoms of AIS?

A

Complete AIS → appear female at birth. Usually present with amenorrhoea, and will have a lack of body hair. The patient will have undescended testes and an absent uterus. Breast development may occur as a result of testosterone conversion to oestradiol.

Partial AIS → present with a varying degree of genital development. This can range from cliteromegaly to ambiguous genitalia

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9
Q

How is AIS diagnosed?

A

Buccal smear or chromosome analysis to reveal 46XY genotype

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10
Q

What is the management of AIS?

A

Counselling - raise child as female

Bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)

Oestrogen therapy

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11
Q

What is 5 alpha reductase?

A

Autosomal recessive condition. Results in the inability of males to convert testosterone to dihydrotestosterone (DHT). (More potent, responsible for external genitalia differentiation)

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12
Q

Define sex determination

A

Sexual determination is a genetically controlled process dependent of the Y chromosome, i.e. it is the genetic determination of male or female. The key gene is the SRY (sex determining region Y), which determines whether a testis or ovary will form. The formation of a testis then regulates sexual differentiation.

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13
Q

Describe the process of sexual differentiation

A

Male - SRY - Sertoli cells develop - produce AMH mullerian duct degenerate.
Leydig cells - testosterone - wollfian duct - epididymis, vas deferens, seminal vesicle, ejaculatory duct .
DHT - external structures

Female - no SRY. Ovary develops. No sertoli cells so no MIS causing mullein duct development and Fallopian tubes, uterus, upper vagina.
no leydig cells - regression of wollffian ducts.

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14
Q

What is adrenarche and menarche?

A

Adrenarche - secretion of adrenal androgens leading to growth of hair, height.

Menarche - onset of menstruation.

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15
Q

Define delayed and precocious puberty

A

Precocious : The onset of secondary sexual characteristics before age of 8 in girls or 9 in boys

Delayed: Defined as the lack of any pubertal signs by the age of 13 years in girls and 14 years in boys.

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16
Q

What are causes of delayed puberty?

A

1Constitutional delay: idiopathic/ within families. Temporary delay due to severe illness in childhood, e.g. mumps.

  1. Organic causes:
    Hypothalamic [Hypogonadotrophic hypogonadism – low levels of LH/FSH and low levels of sex steroids]:
    Congenital GnRh deficiency (e.g. Kallmann’s syndrome – where there is failure in migration of GnRH neurons) or acquired (trauma, surgery)

Gonadal [Hypergonadotrophic hypogonadism– high levels of LH/FSH and low levels of sex steroids]:
Congenital disorders, chromosomal disorders (e.g. Klinefelters) or acquired (e.g. testicular/ovarian torsion, radiation, surgery, infection)

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17
Q

What are causes of precocious puberty?

A

Classification:
1. Gonadotrophin dependent (‘central’, ‘true’) → consonance maintained
• Caused by excess GnRH secretion: either idiopathic (common in females) or secondary (trauma, radiotherapy, intracranial tumour or CNS damage)
• FSH & LH raised

  1. Gonadotrophin independent (‘pseudo’, ‘false’) → loss of consonance
    • Due to excess sex hormones
    • FSH & LH low due to negative feedback
    • Caused by:
    o Ovarian: tumours
    o Testicular: tumours, activating LH mutations on Leydig cells which release testosterone
    o Adrenal: CAH in males
    o Primary hypothyroidism: high levels of TSH acts on LH/FSH receptors causing a release of sex steroids
    o McCune-Albright syndrome: Sx - precocious puberty, café au lait spots, fibrous dysplasia of the bones & short stature
    o Exposure to exogenous steroids
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18
Q

Describe the events of puberty and when they occur

A

Thelarche
Menarche
puberache

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19
Q

What are the stages of the menstrual cycle?

A

Follicular phase → growth of follicles up to ovulation, dominated by oestrogen (variable length)

Luteal phase → formation of corpus luteum, dominated by progesterone production (always lasts 14d)

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20
Q

Outline the hormonal changes in the menstrual cycle?

A
  1. Follicular phase:
    Early in the follicular phase steroids low due to the regression of CL
    FHS released from -ve feedback leading to the intercycle rise in FSH → follicle selection

• Dominant follicle is selected and produces oestrogen which gives –ve feedback causing FSH levels to fall

  1. Mid-cycle:
    • Dominant follicle continues producing oestrogen till levels exceed 300pmol where negative feedback switches to positive
    • This causes an LH surge (and FSH peak)
    • LH induces ovulation
  2. Luteal:
    • Corpus luteum produces progesterone and negative feedback is re-instated
    • Withdrawal of progesterone leads to menses
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21
Q

How does 5 alpha reductase present?

A

Internal male structure are formed, external are not

May appear female or have ambiguous genitalia

Can undergo virilisation at puberty (high levels of circulating testosterone)

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22
Q

What are the causes of oligo/amenorrhoea?

A

Primary: structural or genetic

Secondary
Premature menopause, PCOS, hyperprolactinaemia
Physiological: pregnancy, lactating, pre or post.

Hypothalamic
Primary - congenital reduced GNRH. Secondary - stress, low fat/body weight, exercise

Pituitary
Hyperprolactinaemia, Sheehans

Ovarian
Acquired: PCOS or premature menopause
Congenital: turners
Endocrine; thyroid

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23
Q

How does 5 alpha reductase present?

A

Internal male structure are formed, external are not

May appear female or have ambiguous genitalia

Can undergo virilisation at puberty (high levels of circulating testosterone)

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24
Q

What are the first sign of puberty in girls?

A

First sign is breast development at around 11.5 years of age (range = 9-13 years)
Height spurt reaches its maximum early in puberty (at 12) before menarche
Menarche at 13 (11-15)
There is an increase of only about 4% of height following menarche

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25
What are the investigations and management for precocious puberty?
Investigations: Auxology: accurate measurements of height, body proportions + weight Tanner stage + Ferriman and Gallwey scoring system for hirsutism •Bone age estimation, LH, FSH, Sex steroids, US scan of pelvis, MRI of hypothalamic areas •Measuring adrenal steroids: increased in tumours + in CAH, the precursors of androgens Treatment: dampens down the effects of the sex steroids Anti-androgens 5-alpha reductase inhibitors Aromatase inhibitor – inhibits conversion of testosterone to oestrogen Long acting GnRH analogues – dampens down the pituitary so there is no release of LH/FSH
26
What investigations and management would be needed for delayed puberty?
Same Ix as precocious. + Check anosmia for kallmans. Mx Testosterone/Oestrogen Oxandralone (synthetic steroid) Kallman’s can be treated using pulsatile GnRH as the gonads are still functioning
27
What is the Tanner staging system?
5 stages of development for breasts, pubic/axillary hair and male genitalia
28
Define menopause
Menopause is the permanent cessation of menstruation due to loss of ovarian follicular function. Average age 51. 12 months after the last period in women > 50 years 24 months after the last period in women < 50 years
29
When is menopause classified as premature?
<40
30
What are the symptoms of menopause?
Change in periods Vasomotor symptoms • Hot flushes • Night sweats Psychological • Anxiety/ depression • Short-term memory impairment Urogenital changes • Vaginal dryness and atrophy • Urinary frequency Longer term complications •OP+Heart disease
31
Define dysmenorrhoea
painful periods
32
Define menorrhagia
heavy periods
33
What are the most common causes of oligo/amenorrhoea?
Premature ovarian failure PCOS Hyperprolactinamia
34
What are the most common causes of oligo/amenorrhoea?
Premature ovarian failure PCOS Hyperprolactinamia
35
What investigations are required for oligo/amenorhoea?
Pregnancy: urinary or serum ßhCG Ovarian and pituitary function → FSH + oestrodial (low E2 with high FSH = ovarian problem, low E2 with low FSH = pituitary or hypothalamic) Prolactin, thyroid function tests Androgen levels: raised levels may be seen in PCOS Imaging: USS of vaginal and uterus for structural abnormalities
36
Causes of menorrhagia
DUB Anovulatory cycles ``` Fibroids. Endometrial/Cervical polyps. Endometriosis. Adenomyosis. Endometritis. Pelvic inflammatory disease (PID). Endometrial hyperplasia or carcinoma. Systemic disease: bleeding disorders (Von Willebrand’s), hypothyroidism, liver or kidney disease An IUD (Copper coil! NOT Mirena) ```
37
What investigations are required for menorrhagia?
``` Exclude pregnancy Assess Hb Systemic causes: TFT/ clotting TVUS Biopsy ```
38
What is the management of menorrhagia?
Does NOT require contraception: Tranexamic acid or NSAIDs (e.g. mefenamic acid) Does require contraception: 1st line: Levonorgestrel-releasing intrauterine system (IUS) – Mirena 2nd line: Combined oral contraceptive (COC) 3rd line: Long-acting progestogens (e.g. Depo-Provera) If medical treatment fails the surgery can be considered: Polyp or fibroid removal Endometrial ablation Myomectomy, hysterectomy or uterine artery embolization
39
What are causes of intermenstrual bleeding?
Ectopic pregnancy Anatomical Vagina: adenosine, vaginitis, tumours Cervix: infection, cancer, polyps, ectropion Uterus: polyps, cancer, adenomyosis, fibroids Ovary: bleeding at ovulation Iatrogenic: tamoxifen, smear, missed pills, anticoagulants
40
What investigations are required for IMB?
``` Pregnancy Infection Cervical smear if due! Bloods: FBC, clotting, FSH/LH, TSH TVUS +/- biopsy ```
41
What is the most important cause for PCB?
Cervical cancer
42
What are causes of PCB?
Ectropion (COCP) Cervical Ca Cervical/endometrial polyps Vaginal cancer
43
What are causes of dysmenorrhoea?
Primary - no cause. NSAIDS/COCP ``` Secondary Endometriosis Adenomyosis Pelvic inflammatory disease Intrauterine devices (copper coils. Note mirena may help dysmenorrhoea) Fibroids ```
44
How do you differentiate primary and secondary dysmenorrhoea?
``` 1 absence of pathology begins 1-2 years after periods suprapubic cramping - back and thighs starts just before/within few hours of period NSAIDs are good ``` ``` 2 several years after periods congested/crampy 3-4 days before period and relieved by menstruation refractory to NSAIs ```
45
What is DUB?
abnormal uterine bleeding without any obvious structural or systemic pathology. It usually presents as menorrhagia. The diagnosis of DUB can only be made once all other causes for abnormal or heavy uterine bleeding have been excluded
46
How is DUB treated?
1st line: progestogen (oral or IUD). 2nd line: COCP may be tried if this is insufficient. In patients who do not improve, surgical intervention may be considered
47
What is pre-menstrual syndrome?
Anxiety, stress, fatigue, mood swings during luteal phase. Symptom diary
48
How is pre-menstural syndrome treated?
Exercise, CBT, COCP, SSRI
49
Causes of acute pelvic pain
``` Ectopic Miscarriage UTI Appendicitis Torsion PID ```
50
Causes of chronic pelvic pain
``` PID Endometriosis IBS Ovarian Cyst Prolapse ```
51
Name enzyme inducers/CRAP GPS
``` Carbamazepine Rifampicin Alcohol chronic Phenytoin Grisefolvin Phenobarbitone Sulphonylurea ```
52
How does an ectopic present?
6-8 weeks no period abdo pain and PVB Shoulder tip Cervical excitation
53
How does PID present?
``` Pelvic pain deep dyspareunia discharge fever dysuria cervical excitation ```
54
How does ovarian torsion present?
Sudden onset unilateral pain N&V Tender adnexal mass
55
How does a miscarriage present?
Vaginal bleed and cramps pain after period of amenorrhoea
56
How does endometriosis present?
Chronic pelvic pain dysmenorrhoea - starting few days before bleed pain during sex sub fertility
57
how does an ovarian cyst present?
Unilateral dull ache - intermittent or during sex torsion or rupture may cause severe pain some cause swelling/pressure effects on bladder
58
How does urogenital prolapse present?
Heaviness, dragging, bearing down | Urinary symptoms
59
What are causes of superficial dyspareunia?
Dermatological conditions → atopic dermatitis, contact dermatitis Infection → vulvovaginitis, herpes simplex, interstitial cystitis Mucosal dysfunction → reduced secretion, e.g. due to irradiation or medications Structural abnormalities → imperforate hymen, perineal injury MSS disorders → vaginisimus (spasm)
60
What are causes of deep dyspareunia?
Infection/inflammation → PID, cervicitis Structural → fibroids, adenomyosis, endometriosis MSS → levator ani spasm
61
Define endometriosis
growth of ectopic endometrial tissue outside the uterine cavity
62
What causes endometriosis?
Oestrogen dependence reduces in pregnancy and menopause higher levels of exposure increase chance
63
Symptoms of endometriosis
``` Chronic pelvic pain – often cyclical Dysmenorrhoea – pain often starts days before bleeding Deep dyspareunia Subfertility Urinary symptoms e.g. dysuria, urgency Dyschezia (painful bowel movements) ```
64
What is the treatment for endometriosis?
``` NSAIDs COCP Progestogens GnRH analogues e.g. goserelin- said to induce a 'pseudomenopause Intrauterine system (Mirena) ``` Laparoscopy to ablate or hysterectomy last resort
65
Advantages and disadvantages of the COCP?
Reduces risk of endometrial. ovarian and CRC Increases risk of VTE, breast, cervical cancer Temporary symptoms of nausea, headache, breast tenderness
66
COCP missed pills
``` if 1. - take next if 2 - W1 may need emergency if had sex in PFI or W1 W2 continue W3 next pack ```
67
What are the CI to COCP?
>35yrs old and smoking more than 15 cigs/day Migraine with aura Hx of VTE, stroke, IHD Breast feeding <6 weeks post-partum Uncontrolled HTN Current breast cancer Major surgery with prolonged immunisation
68
What are progresterone like side effects?
breakthrough bleeding, weight gain, breast pain and PMS-like symptoms. It is generally used where the COCP is contraindicated (e.g. lactating mothers).
69
What are the contraindications for progesterone pills?
Undiagnosed PVB | Severe arterial disease
70
CI to IUD?
Gynaecological cancer Undiagnosed pelvic bleeding Infection Pregnancy
71
What is kallmans syndrome?
Hypogonadotrophic hypogonadism - failure of GnRH neurones to migrate to hypothalamus
72
What are the symptoms in Kallmans syndrome?
``` Anosmia Delayed puberty low sex hormones low LH/FSH tall cleft lip/palate ```
73
What is Klinefelters?
``` Often taller Lack of secondary sexual characteristics small firm testis inferti;e gynaecomastia raised gonadotrophin evils Primary hypogonadism chromosome analysis to diagnose ```
74
What is Turners syndrome?
``` Short Webbed neck bicuspid valve primary amenorrhoea high arched palate horses kidney hypothyroid affects females ```
75
What is Noonan's syndrome?
Male turners | similar features of webbed neck, widely spaced nipples, short, pacts deformity.
76
State signs and symptoms of PCOS
``` Menstrual problems - oligomenorrhoea, amenorrhoea Hirsutism, acne - androgens Obesity Acanthosis nigricans Subfertility ```
77
Outline the endocrine abnormalities in PCOS
``` Androgens Insulin sensitivity Raised LH:FSH ratio Testosterone raised LH high LOW shbg ```
78
Link between PCOS and insulin resistance
Impaired glucose tolerance and metabolic syndrome
79
Investigations for PCOS
``` Pelvic USS - >12 cysts FSH, LH, PRL, Testosterone Glucose Raised insulin high LH ``` Dexamethasone DHEA-S CT/MRI Venous sampling if tumour suspected
80
Management for PCOS
``` Weight Periods - pill Hirsutism /Acne - COCP, TOPICAL EFLORNITHINE, SPIRO Infertility treatment - metformin, clomiphene, GnRH, diathermy, IVF ```
81
Causes of Hirsutism
``` PCOS Cushings CAH Androgen therapy obesity - insulin resistance Adrenal tumour Androgen secreting ovarian tumour phenytoin, steroids Prolactin Ovarian hyperthecosis - non malignant secreting of testosterone form theca cells ```
82
High testosterone in female
PCOS CAH Tumour
83
Management of hirsutism
``` Weight loss cosmetic COCP Topical eflornithine for facial hirsutism Spiro/finasteride ```
84
How is the contraceptive patch used?
3 weeks on, 1 week off - bleed Same delay idea - less then 48 hours continue/change as usual. If delay of putting on a patch is more than 48 hours - change patch, barrier contraception 7 days. If sex occurred during last 5 days or patch free time emergency contraception If delay in removing patch at the end of week 3 fine just remove.
85
What are the types of emergency contraception?
Levonorgestrel Ulipirstal (ellaOne) IUD
86
Use of IUD for emergency contraception
Inserted within 5 days of UPSI | Can leave long term or remove after first period
87
Use of ellaone as emergency contraception
<120 hours
88
Use of levonorgestrel as emergency contraception
<72 hours | if vomit within 3 hrs need to repeat dose
89
What is the IUD vs IUS
IUD - copper, immediately works | IUS - hormonal, works after 7 days
90
Post-partum contraception
Need after 21 days POP start anytime even if breastfeeding COCP >6 w pp if breastfeeding IUD within 48 hrs of birth or >4 weeks
91
Patient with +HPV sample, when would she need a repeat smear
12m

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