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Part 2 > Adolescent Gynaecology > Flashcards

Adolescent Gynaecology Flashcards

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1
Q

HMB

A

most commonly due to anovulatory cycles

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2
Q

Sheehan Syndrome

A

5 in 100000
1- Severe PPH
2) Hypovolemic shock
3) ischaemic necrosis of anterior Pituitary

agalactorrhea
amenorrhea
hypothyroid
adrenal insufficiency/crisis

Lose- TFTs, LH, FSH, ACTH, PL

Treatment:
levothyroxine
GH
hydrocortisone
HRT

Sheehan= Ss
Shock, Severe PPH iSchaemic necrosis

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3
Q

MRKH

A

46XX
Mullerian agenesis
short vagina (no cervix/womb)
ovaries present

dilation/surgery for RVI
surrogacy for pregnancy

sporadic inheritance, ?AD with incomplete penetrance

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4
Q

Physiology of puberty- F

A

F= aged 8-14

1) Nocturnal GnRH pulsatility increase
2) Loss of diurnal range
3) +ve feedback of E on GnRH
4) LH Surge

90% cycles anovulatory
multicystic appearance of ovaries

Increased FSH = increase E = oogenesis
=LH = increase P

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5
Q

Stages of Puberty

A

1) Thelarche (age 9-10)
E- breast buds and ducts/alveoli
P- increase number of lobules

2) Pubarche
hair in axilla-> 2 years -> hair in genitals
testosterone-mediated (independent of HPO)

3) Menarche
1.5-3 years after thelarche
LH and FSH (median 12.8 yrs)

4) Growth Spurt
Estradiol, GH, and ILGF-1

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6
Q

Physiology of puberty- M

A

10-16 yo
GnRH pulse changes as per F

1) Leydig and Sertoli cells increase testicular size
2) first ejaculation (may not be fertile for 1 year)
-pubarche 12 months after

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7
Q

Tanner Staging

A

1= prepubertal
2=pubertal changes
5= adult

M genital size
growth
pubic hair
breast development

2= entered puberty

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8
Q

Precocious Puberty- F

A

<8 yo

Gonadotrophin dependent (central)
raised GnRH, LH and FSH
-mostly idiopathic (75%)
CNS changes/lesions, infections, radiation
can be secondary to peripheral causes

Gonadotrophic independent
autonomous sex steroid secretion
raised E independent of Gonadotrophins
difficult to treat
tumors, CAH, Cushing’s, adrenal,

Iatrogenic
creams/steroids

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9
Q

Investigation for precocious puberty

A

XR wrist (fused by raised E) >2 years= precocious puberty
USS pelvis
Cranial MRI (central)
Adrenal MRI

FSH, LH, E2, 17 hydroprogesterone
TFTs, GnRH stimulation, ACTH
Urinary steroid profile (adrenal androgens)

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10
Q

Delayed Puberty- F

A

no breasts age 13 or
no menses age 15 if other signs

r/o
constitutional delay
low BMI
chronic disease
too much exercise

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11
Q

Types of delayed puberty

A

3%
M>F

hypogonadotrophic
low GnRH, LH, FSH
disorder of hypothalamus/pituitary
chronic illness/stress

hypergonadotropic
high LH and FSH
gonadal disorder- no response to gonadotropins
Turner’s, dysgenesis

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12
Q

Investigation for delayed puberty

A

LH, FSH, TFTs, T, PL
Karyotyping
tanner staging/BMI

FHx

USS, MRI (especially if PL >1500)
XR wrist

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13
Q

CAIS

A

XY
Normal testosterone and DHT but unresponsive to androgens
breasts (T converted to E)/unusual or female external genitalia
no uterus, undescended testes
-no hair/menstruation

partial- androgen receptor defective
complete- absent receptors

Wolffian’s degenerate, no mullerian as normal AMH

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14
Q

Turner’s

A

45X
short stature
POI
May enter puberty but full secondary sex characteristics are rare
cardiac/renal changes
webbed neck, wide spaced nipples, streak ovaries

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15
Q

Klinefelter’s

A

47XXY
Most common DSD

Infertility/gynaecomastia
irregular sexual maturation
1 in 500M

rs= breast

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16
Q

Swyer Syndrome

A

46XY (changes to SRY gene)
no SRY/AMH/T
mullerian/extragenital -> F
gonads- small undeveloped testes -> M

streak gonads
risk of gonadoblastoma
induce puberty and give HRT

swy= SRY

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17
Q

5 alpha reductase deficiency

A

XY
normal testosterone, low DHT
abnormal external genitalia, virilisation at puberty
autosomal recessive

normal Wolffian, mullerian degenerate

No DHT dependent processes (external genitalia from urogenital sinus)
-no acne/balding/beard (DHT)
T= testes descend, voice deepens, penis lengthens, muscle mass

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18
Q

Trigger for puberty

A

LH and FSH suppressed by continuous GnRH secretion
pulsatile= puberty (unknown trigger)

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19
Q

Male embryology

A

SRY gene of Y chromosome activated at 6 weeks
Sertoli cells=AMH=involution of mullerian duct
Leydig cells- testosterone
Wolffian duct- epididymis, vas deferens, seminal vesicles

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20
Q

Genitals at 6 weeks

A

bipotential gonads
mullerian duct
wolffian duct

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21
Q

Female embryology

A

reduced AMH and testosterone
Wolffian regresses
Mullerian:
uterus, cervix, tubes, upper 1/3 vagina

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22
Q

Genital tubercle- testosterone

A

5 alpha reductase converts testosterone to dihydrotestosterone
tubercle= glans penis
folds= shaft
swelling= scrotum

by 12 weeks

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23
Q

Genital tubercle- no testosterone

A

tubercle= clitoris
folds= labia minora
swelling= labia majora

Tubercle=cliToris

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24
Q

Primary amenorrhoea- diagnosis

A

No menses at:
age 15 if secondary sex characteristics
age 13 if no secondary sex characteristics

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25
Primary amenorrhoea- investigations
No breast development: FSH high: gonadal dysgenesis PI Turner's Swyers Low/normal: constitutional/weight/illness Kallmann's pituitary Breasts: USS no uterus- AIS/Mullerian uterus- obstruction/PCOS
26
Hyperprolactinaemia
>1500 x 2= MRI low FSH, LH and Estrogen tumor, stress/starvation, hypothyroid, PCOS, liver/kidney Ask about: headache, visual changes, galactorrhoea
27
low BMI
<19 low leptin low GnRH | low= low
28
Cushing's
Raised ACTH Can delay/arrest puberty ACTH from anterior puberty-> reduced gonadotrophins, GH etc
29
Constitutional delay- results
bone scan shows delayed maturation follicles on USS reassure and f/u check maternal hx
30
Kallmann's
M>F, rare X linked congenital absence of GnRH can be inherited also have anosmia and colour blindness delayed/absent puberty, treat with hormone replacement
31
Gonadal dysgenesis
Hypergonadotrophin hypogonadism Turner's Swyer's POI r/o RT/CT thyroid genetic infections addison's
32
Uterine agenesis
MRKH unknown aetiology normal urogenital sinus (ext gen) no mullerian may have renal/vertebral changes primary amenorrhoea but otherwise normal puberty normal HPO axis 46XX Have ovaries (paramesonephric)
33
Types of mullerian changes
30% association with renal changes U0= normal U1= dysmorphic, T shaped cavity U2=circuate/septate U3=bicorporeal U4= hemiuterus (separate halves) U5= aplastic (nothing or unjoined half)
34
Congenital Adrenal Hyperplasia
spectrum of enzyme changes changes to adrenal steroidogenesis
35
CAH- 21-OH deficiency
>90% of cases adrenal steroids shunted into androgen pathways -75% salt wasting (low BP, reduced mineralocorticoids) 46XX- virilised external genitalia at birth, virilisation/amenorrhoea at puberty low cortisol and aldosterone rx= give hydrocortisone and fludrocortisone
36
Primary amenorrhoea- investigation
U+Es E/T/SHBG/FSH Prolactin USS TFTs Karotyping
37
Adolescent PCOS diagnosis
Must be at least 2 years after menarche
38
Vulval changes in adolescence
irritation: reduced estrogen= reduced lactobacilli labial fusion: normal, may resolve or can give topical oestrogens do not operate
39
Ovarian changes in adolescents
60% cysts are functional <7cm- surveillance only
40
Granulosa cell tumors
50% ovarian malignancies in adolescents raised E= pseudo precocious puberty
41
Gonadoblastoma
rare, gonadal changes due to Y chromosome benign but can become malignant
42
Contraception for behavioural changes
consider: immobility DVT risk enzyme inducers swallowing BMD can use if significant distress and educational/symptomatic treatments exhausted
43
Court of Protection decisions
disagreements, finely balanced serious interference of rights eg: -sterilisation -tissue donation -contraception covertly administered -experimental/innovative treatments
44
HMB in adolescents
hypothryoid Down's catamenial epilepsy same ixn and treatments
45
Fragile X
X linked dominant M worse affect than F neurodevelopment changes, physical features and macro-orchidism at puberty
46
Hormones in puberty-F
FSH- stimulate follicles LH- acts on theca cells to stimulate androgen production, converted to oestrogen by aromatase from granulosa cells Rising E= breast development growth of genital tract thickened endometrium pubertal growth spurt
47
Adrenarche
6-8 years activation of adrenal glands- increased DHEA/DHEAS body odour, acne, oily skin independent of HPO
48
Precocious puberty -M
before age of 9 central (Gn dependent, premature HPG activation) Peripheral (GN independent- HPG not involved)
49
McCune-Albright Syndrome
Triad of: Cafe au lait spots fibrous dysplasia endocrine hyperfunction presents as **Gn independent** precocious puberty rx- suppress gonadal steroidogenesisis with **aromatase inhibitors**
50
Ovarian tumors and precocious puberty
Granulosa cell- oestrogen Sertoli-Leydig cell- androgen
51
Hypothryoid and puberty
very high T**SH** reacts at F**SH** receptors can be delayed/precocious
52
GnRH stimulation test
Give GnRH -LH dominance -pubertal response (HPG activated, central) FSH dominance -pre-pubertal response (HPG not activated, peripheral) | LH dominance-> LH triggers ovulation so pubertal/central. prepubertal=pe
53
Why treat precocious puberty?
halt/regress secondary sex characteristics prevent early menarche halt skeletal maturation (improve final height) avoid psychosexual/behavioural sequelae
54
Treatment of central precocious puberty
GnRH analogues downregulates GnRH receptors, reduces Gn synthesis greatest benefit to final height if <6yo
55
Treatment of peripheral precocious puberty
treat cause eg hypothyroid- replace t4 exogenous steroids- discontinue course
56
Treatment of delayed puberty
treat underlying cause (eg disease/thyroid) Reassure if normal growth/bone age Low dose E to initiate breast/growth/bone (2.5-5mcg/d po EE, over 12-18 months) psychological support
57
17b HSD3 deficiency
no androstenedione conversion to testosterone female/ambiguous genitalia at birth then virilisation at puberty due to peripheral conversion
58
LH receptor defects
Leydig cells cannot respond to LH testosterone deficiency similar to CAIS but no breasts as no androgen to E conversion
59
Mullerian duct fusion
at 9 weeks and septum should be reabsorbed to make one cavity
60
Arcuate uterus
indentation <1cm
61
bicornuate uterus
indentation >1cm failure of fusion of ducts septum= failure of resorption
62
Well developed breasts, scant hair primary amenorrhea, normal ext gen USS= absent uterus and undetectable ovaries
CAIS
63
Neonate with ambiguous genitalia USS= Mullerian and Wolffian structures 46XX karyotype
Ovotesticular DSD
64
Adolescent raised as F Primary amenorrhoea clitoromegaly, minimal breasts/hair virilisation at puberty High T, low DHT 46XY
5 alpha reductase deficiency
65
2 endometrial cavities and cervices
uterus didelphys
66
contraception before menarche
condoms HC not recommended LNG-EC/CuIUD
67
Hirsutism Score
Ferriman and Gallwey 0=nil 4=extensive

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