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Gynaecology > General > Flashcards

General Flashcards

1
Q

Primary Amenorrhoea - Causes

A
  • Chromosomal 50%
  • Hypothalamic 20%
  • Mullarian 15%
  • Anatomic 5%
  • Pituitary 5%
  • Other 5%
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2
Q

Primary amenorrhoea - Definition

A
  • No menses by 15 with normal secondary sex characteristics

- No menses by 13 without secondary sex characteristics

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3
Q

Hypergonadotrophic primary amenorrhoea - Causes

A 
Turner’s syndrome
Structurally abnormal X chromosome
Pure gonadal dysgenesis
Enzyme deficiencies
Mosaicism
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4
Q

Hypogonadotrophic primary amenorrhoea - Causes

A

Physiological delay
Kallmans syndrome
CNS tumours
Chronic disease

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5
Q

Amenorrhoea with secondary sex characteristics

A 
ANATOMIC:
- Hymen
- AIS
-True Hermaphrodite
NON-ANATOMIC
- Ovarian insufficiency
- Iatrogenic
- Autoimmune
- Glalactoaemia
- Savage syndrome (Gonadotrophin resistant ovary)
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6
Q

Secondary amenorrhoea - Causes

A
  1. Pregnancy
  2. Ovarian 40% (PCOS, prem insufficiency [chemorad/turners/autoimmune/fragile x premutation])
  3. Hypothalamic 35% (functional, infiltrative)
  4. Pituitary 20% (prolactinoma, sella mass, sheehans, radiation)
  5. Uterine 5%
  6. Thyroid dx
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7
Q

Delayed puberty

A
  1. Anatomic - Rokitanski, obstruction
  2. Hypergonadotropic
    - Gonadal dysgenesis (turner’s, 46XX, 46 XY)
    - Early gonadal failure
  3. Hypogonadotrophic
    - Constitutional
    - infiltrative lesion
    - Kallmans (anosmia and colour blindness)
    - chemorad
    - hypothyroidism
    - drugs
    - Chronic disease
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8
Q

Precocious puberty - Causes

A
  1. CENTRAL
    - Idiopathic
    - Tumours
    - Infection
    - Trauma
    - Congenital abn e.g. hydrocephalus
  2. PERIPHERAL
    - HYPOgonadotrophic
    * isosexual = oestrogenic neoplasm (e.g. McCune albright [fibrous dysplsia, cafe au lait patches and hyperfunctioning endocrinopathies])
    * heterosexual = androgenic tumour or CAH
    - HYPERgonadotropic
    * GnRH or BHCG [similar to LH] secreting tumour

*** Premature adrenarche may be the first sign of PCOS

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9
Q

Precocious puberty - Definition

A

Development of secondary sex characteristics earlier than expected i.e. 2SD < mean. Usually 8 in girls and 9 in boys.

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10
Q

Endometriosis - Level A evidence for Infertility

A
  • Rx grade I/II with excision or ablation
  • No role for hormonal therapy (either primary or adjunct to surgery)
  • Endometriomas:
  • no benefit to remove if >3cm in ART context
  • if removing cystectomy is better than drainage
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11
Q

Endometriosis - Other levels of evidence for Infertility

A

B:
- GnRH for 3-6/12 prior to ART improves clinical pregnancy
C:
- Stage III/IV laser coat better than monopolar in sport pre rates
- IUI and ovarian hyperstim increases live birth rates )Stage I/II)
- Recurrence not increased by IVF/ICSI

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12
Q

Endometriosis - Level A evidence for Pain

A
  • Progestagens and antoprogestagens effective
  • GnRH antagonists (Groerelin) + add back effective
  • Endometrioma:
  • COCP for secondary prevention
  • cystectomy > drainage
  • Surgery:
  • No role for preop or post op hormonal Rx
  • DO NOT use LUNA
  • Mirena 1-2y secondary prevention dysmenorrhoea
  • Presacral neurotomy is difficult but effective
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13
Q

Endometriosis - Other levels of evidence for Pain

A

B:
- COCP
- Mirena IUD
- Surgery for deep end, but 2% intro complication rate
- Aromatoase inhibitors (w Prog, COCP or GnRH ant)
- Endometrioma - excision lower recurrence rate
C:
- Ring or patch
GPP:
- Hysterectomy for those who’ve completed their family and have failed medical therapy

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14
Q

Components of the prognostic scoring system for persistent trophoblastic disease

A
  • Age = old worse
  • BHCG level = higher worse
  • Outcome of index pregnancy = term worse than MC worse than molar preg
  • Time from index pregnancy = longer has worse outcome
  • Size of residual tissue = bigger is worse
  • Metastatic disease = liver/brain worse than GIT worse than spleen/kidneys worse than lungs
  • Previous CTX (double agent worse than single)

Will guide decision of MTX or EMA-CA or EMA-EP +/- RTx.

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15
Q

XY Females

A
  • AIS (no androgen receptors so no hair)
  • Gonadal dysgenesis (NO secondary sex characteristics)
  • 5 alpha reductase deficiency (No DHT so no prostate/penis, but male secondary sex characteristics)
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16
Q

Requirements for Gillick Competence

A
  • Unable to convince parents
  • Likely to engage in sexual activity regardless of contraception
  • Able to understand advice given
  • Contraception required for physical or mental health
  • In the patients best interest
  • No lower age limit
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17
Q

PCOS - Rotterdam Criteria

A

2/3: *need all 3 in adolescents

  • Polycystic ovaries (>11 follicles in EACH ovary, 2-9mm, OR >10mL)
  • Hyperangrogenism (clinical or biochemical)
  • Oligoamenorrhoea

Present in 15% of women.

18
Q

PCOS - Pathogenesis

A

Incompletely understood
Complex hormonal and biochemical alterations
- Genetics (70%) and environmental
- Increased LH and LH pulse frequency, and enhanced ovarian sensitivity to LH
- Increased insulin resistance > increased androgens and decreased SHBG

19
Q

Pregnancy risks of PCOS

A

GDM (~50%)
Miscarriage (mostly secondary to obesity)
PIH
SGA

20
Q

Long term risks of PCOS

A
  • Endometrial cancer RR 2.7
  • Type II DM RR 4
  • CV disease
  • OSA
  • Anxiety/depression
21
Q

Differential diagnoses for PCOS

A
  • Hyperprolactinaemia
  • Cushings disease
  • late onset CAH
  • Hypothyroidism
  • Androgen secreting adrenal tumour
22
Q

Congenital Adrenal Hyperplasia - Presentation

A
  1. Classical
    - Virilised female baby
    - Hyponaturamia and hyperkalaemia secondary to aldosterone deficiency
  2. Non-classical
    - Precocious or normally times heterosexual puberty
    - PCOS like syndrome
23
Q

Congenital adrenal hyperplasia - Mechanism

A

21-hydroxylase is the most commonly affected enzyme
Usually converts 17-OH-progesterone to 11-deoxycortisol > cortisol (and aldosterone). (17-OH-P is also the substrate for androstenedione).
Without cortisol no negative feedback, so higher ACTH and more substrates into androstenedione.

24
Q

Congenital adrenal hyperplasia - Rx

A

Dexamethasone/Prednisone for pathway supression
COCP
Ovulation induction if required

25
Q

When should AN thromboprophylaxis start?

A

As early in pregnancy as practically possible.

26
Q

Women w one previous unprovoked DVT without any thrombophilia?

A

Close surveillance only AN.

Consider 6/52 post partum.

27
Q

Which thombophilias need AN thromboprophylaxis?

A

Antithrombin III
Factor V Leiden homozygotes or compound heterozygotes
More than one thrombophilia

28
Q

Prevalence of post hysterectomy vault prolapse

A

12% if hysterectomy for prolapse

2% if performed for other indications

29
Q

Prevention of vault prolapse at the time of hysterectomy

A
  • McCall culdoplasty at the time of hysterectomy (approximating the USL)
  • sacrospinous fixation if the vault descends to the introits during hysterectomy
30
Q

Reversible causes of urinary incontinence

A 
DIAPPERS
Delirium
Infection
Atrophy
Psychological 
Pharmacological
Excessive urine production
Restricted mobility
 Stool impaction
31
Q

Cause of urinary urge incontinence

A

Idiopathic

Neurogenic e.g. DM, MS, CVA

32
Q

Conservative Rx urge incontinence

A
  1. Lifestyle modification (fluid, ETOH, caffeine, constipation, mobility, toilet access)
  2. Bladder training
  3. Supervised physiotherapy
  4. Electrical stimulation w TENS
  5. Pessary of large cystocoele present
33
Q

Pharm Rx urge incontinence

A

Oestrogen (improved symptoms, improved UDS)
Anticholinergics (15% greater than placebo) e.g Ditropan, Detrusitol
TCA (anticholinergic and LA) e.g. Imipramine
Intravesical botox

34
Q

Surgical Rx urge incontinence

A

Hydrodistention

Sacral nerve stimulation

35
Q

What is the PALM COEIN classification and it’s components?

A

Classification system of abnormal uterine bleeding.
4 structural
4 other
1 underfined

Polyp
Adenomyosis
Leiomyoma (submucosal, other)
Malignancy and hyperplasia

Coagulopathy
Ovulatory
Endometrial
Iatrogenic

Not yet classified

36
Q

What is the risk of miscarriage by maternal age?

A

45 95%

GTG

37
Q

What are the diagnostic criteria for APLS?

A

Antibodies - postivie x 2 at least 10 weeks apart
Anticardiolipin
Lupus anticoagulant
B2 glycoprotein

and. ..
- 3 1st trimester losses
- 1 > 10/40 loss w a morpholgically normal foetus
- Delivery <34/40 for placental disease

OR hx thrombotic disease

38
Q

How does APLS cause adverse pregnancy outcomes?

A
  • Inhibition of trophoblast function and differentiation
  • Activation of complement at the materno-foeto interface resulting in local inflammation
  • Thrombosis at the materno foetal interface (later effect)

(first 2 reversed by Heparin!)

39
Q

Preconception or 1st AN Ix in prepreg DM

A
  • UEC
  • Urine MCS
  • HbA1c
  • TSH
  • 24h urine protein/ PCR
  • Opthal consult
  • ECG
  • Assessment of exercise tolerance and CV disease
40
Q

How effective is the Fluvax?

A

~50%, thus still need to Rx women w Oseltamivir

Is 80% effective at preventing hospitalisation

Gynaecology (2 decks)

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