Mrcog PDF
Mrcog PDF
Mrcog PDF
Contents
Contributors
ix
Introduction
xi
xiii
xv
1.
2.
3.
4.
5.
Developmental gynaecology
1.1
1.2
Paediatric gynaecology
Normal and abnormal development of the genital tract:
intersexuality and primary amenorrhoea
Gynaecological surgery
19
2.1
21
Gynaecological surgery
29
3.1
3.2
3.3
3.4
31
35
39
47
59
4.1
4.2
4.3
4.4
61
70
74
80
Urogynaecology
85
5.1
5.2
87
95
vi
6.
7.
8.
9.
Gynaecological oncology
105
6.1
6.2
6.3
6.4
6.5
107
111
114
120
128
Early pregnancy
133
7.1
135
147
8.1
8.2
149
Antenatal management
9.1
9.2
9.3
9.4
9.5
9.6
153
163
165
179
185
190
196
203
215
217
221
230
234
242
246
251
CONTENTS
Induction of labour
Second stage of labour
Caesarean section
Obstetric anaesthesia
Problems in puerperium
271
273
279
292
296
305
307
317
319
vii
xv
2.
Prepare thoroughly.
3.
Read constructively.
4.
5.
6.
1.
2.
Prepare thoroughly.
a.
If you dont know enough, you fail! Obvious and basic. Talk to trainees
who have recently passed the exam. What did they read? What courses
did they attend and how useful were they? Make use of all learning
opportunities within your department and further afield.
It is crucial that you know everything the RCOG has produced: GreenTop guidelines etc. You can access all of this on the section guidelines
on the College web page: www.rcog.org. Similarly, NICE produces
guidelines, www.nice.org.uk. The RCOG and NICE advice are the most
important and must be known well enough for you to refer to it in the
essays and use it to answer MCQs.
xvi
b.
c.
d.
e.
f.
g.
xvii
There are stacks of books written specifically for the MRCOG, e.g.
MRCOG Revision Made Easy by Ngwenya and Lindow and Extended
Matching Questions for the MRCOG, edited by Singh; both texts
published by PasTest. These give good insight into the exam and are
inexpensive. The more you practise MCQs, EMQs and essays the better.
i.
j.
Read constructively.
The immediate conclusion from the above might be that the task is
impossible! It isnt, but it means that your reading has to be disciplined. It
is also evident that you cannot read most things more than once. Hence,
xviii
you need a technique that allows you to capture all of the important
information at the first sitting. Ideally this should be in a format that
facilitates revision so that all of the information is securely stashed in
your head and available for the exam. You cant just read and hope that
everything relevant will stick.
My advice is that you use cards postcard-size or slightly smaller. Big
enough to contain the information you want, but small enough to carry
in a pocket, so that you can go through them whenever you have a
spare moment at work. For example, you might make out a card on
postmenopausal bleeding and the risk factors to elicit in the history. On
the front of the card you would write the title, Postmenopausal bleeding
with a sub-text, Risk factors to elicit from the history. You would then
make out a list of all the things you feel should be included. There would
be obvious things such as the frequency and duration of the bleeding,
associated symptoms like discharge or pelvic pain, a history of treatment
for gynaecological malignancy or pre-malignancy etc. You would include
the increased risk with unopposed oestrogen and the reduced risk with
continuous, combined HRT. Family history would include the possibility
of the woman being from a HNPCC family etc. Once you had compiled
your list on the back, you would count the items and put the number on
the front, so that when you use the card for revision, you read the front
and have to try to recall all of the headings on the back. This book has
been written in a manner that can be re-read on several occasions and
provides a format for remembering the facts.
There are several values to this system. You have to read analytically to
ensure that you have captured all of the important points in whatever you
are reading. Often when we are reading we are only half concentrating.
You cant do this if you have to make out cards. Once you have made
out your cards, you do not need to read the source again. You should
then revise the cards time and again until they are memorised and their
contents are easily recalled.
k.
xix
With EMQs read what the question is about and then the lead in.
You should then have a pretty good idea of what the answer is. You
can then read the list of options. There will probably be one or two
answers close to what you thought the answer should be. The hard bit
is deciding which the best option is. You might have to do a bit of lateral
thinking. A recent question was along the lines of a woman admitted at
28 weeks with significant hypertension and features of PET. A question
was whether she should first have a hypotensive drug or magnesium
sulphate. For most people it was a daft question as you would administer
both. However, it you think it through, the biggest risk to her health is
intracranial haemorrhage from bleeding due to hypertension.
For the essays, you should prepare as many model answers as you
can. See the section below on spotting questions and prepare model
answers for anything you think likely.
Take the subject postmenopausal bleeding. You should be able to
write a model essay on A woman of 55 presents with postmenopausal
bleeding. Critically evaluate the investigation. Write model answers on
all of the questions you think are likely. Make sure that the model answer
can be written in about twenty minutes and on one piece of paper. Dont
write a textbook, it will not avail you in the exam!
Many of the patients you meet in clinical practice will have problems that
could form the basis of an essay. Make a note of the problem and write
an essay. This first thing to do is to make out a plan. Write all the things
you believe to be important. The idea is to get ten or so headings. In
the exam each of these will attract one or more marks, so you can be
confident of a pass.
In the exam itself, spend the first five minutes reading the question
carefully and several times. The examination committee will have
worded it carefully to ensure that the subject can be covered in the
time you have. So the question above on PMB excludes treatment
and there would be no marks for anything you wrote about it. A
classic essay question was the first one to appear in the exam about
domestic violence. The question detailed a woman attending the
antenatal clinic with multiple bruises. It went on to say that full medical
and haematological investigation were normal and to ask about the
management. I marked this question and the pass rate was abysmal.
Most people ignored the advice about the investigations being normal
and repeated all the tests they would do. For which endeavours they got
no marks!
xx
l.
1
Developmental
gynaecology
DEVELOPMENTAL GYNAECOLOGY
1.1
PAEDIATRIC GYNAECOLOGY
1.1.1
Prepuberty
Vulvovaginitis
Early in neonatal life the high postpartum levels of oestrogen protect the
vagina from infection. Shortly after, the fall in circulating oestrogens renders
the vaginal epithelium exposed to opportunistic bacterial colonisation. This is
compounded by poor hygiene, the neutral pH and lack of lactobacilli.
The causes of vulvovaginitis are summarised in Table 1.1. Non-specific
bacterial contamination is the most common diagnosis, with dermatitis and
fungal infection being less common. The clinician should approach with
caution if sexual abuse is suspected.
Bacterial
Viral
Candida
Dermatitis
Foreign body
Sexual abuse
Enuresis
Table 1.1: Causes of vulvovaginitis
Management
On examination careful inspection of the vulva and vagina is necessary.
Swabs may be taken, however discharge is most likely to be due to nonspecific infection or faecal contamination. Occasionally examination under
anaesthetic may be required to remove foreign objects. Parents should be
reassured of the benign nature of the discharge and the absence of longterm sequelae. Parents should also be advised of good hygiene and washing
with gentle soaps and avoidance of excessive cleansing. Occasionally during
acute attacks the use of barrier creams may become necessary as micturition
may be painful.
Labial adhesions
Adhesions of the labia is a benign condition that usually resolves
spontaneously on activation of the ovaries and the production of oestrogen.
This condition usually manifests in early childhood as a result of a hypooestrogenic state. Parental reassurance and the use of topical oestrogens for
2 weeks usually resolve the problem. Careful history taking should rule out
sexual abuse, which may occasionally present in this way.
1.1.2
Puberty
DEVELOPMENTAL GYNAECOLOGY
1.1.3
Adolescence
Menorrhagia
The definition of menorrhagia is a loss of greater than 80 ml. This is extremely
difficult to quantify and personal perception varies considerably. Many
patients are seen as school work is affected and examinations are looming.
If there is doubt then a haemoglobin concentration may prove to be useful
and reassurance given in the absence of anaemia. If anaemia is confirmed
the most successful form of treatment is use of the oral contraceptive pill,
however exclusion of bleeding disorders, especially if a positive family history
is found, is important.
Dysmenorrhoea
Dysmenorrhoea usually responds to simple analgesia and use of the
oral contraceptive pill. In some patients who have severe or refractory
dysmenorrhoea then the clinician should be alert to anatomical anomalies
which may lead to partial obstruction of menstrual flow. In some patients
endometriosis may be the problem and laparoscopy warranted.
1.1.4
Primary amenorrhoea
DEVELOPMENTAL GYNAECOLOGY
1.1.5
Conclusion
&
1.2
1.2.1
Normal development
Gonadal differentiation
Initially, the gonads appear as a pair of longitudinal ridges (the genital or
gonadal regions) and are formed by proliferation of the coelomic epithelium.
Germ cells do not appear in the genital regions until the sixth week of
development. These primordial germ cells appear in the endoderm of the
yolk sac and migrate by amoeboid movement and invade the genital ridges.
Non-development of the gonads occurs if there is failure of the germ cells to
reach the genital ridges. Primitive sex cords then form from proliferation of
the genital ridge. At this stage it is impossible to determine between the male
and female gonad and this is known as the indifferent gonad. Simultaneously,
the two Mllerian (paramesonephric) ducts also appear lateral to the Wolffian
ducts and the cloacal membrane and folds are separated into the anterior
urogenital and posterior anal parts.
In the male fetus the primitive sex cords continue to proliferate and penetrate
deep into the medulla to form the testis or medullary cords. Later, the testis
cords lose contact with the surface epithelium and are separated by a dense
layer of fibrous tissue, the tunica albuginea. By the fourth month the testis is
now composed of primitive germ cells and sustentacular cells of Sertoli. The
interstitial cells of Leydig develop from the mesenchyme located between the
testis cords. It is not until puberty that the cords then acquire a lumen forming
the seminiferous tubercles.
In the female, the primitive sex cords are broken up into irregular cell clusters.
Later these clusters disappear and are replaced by vascular stroma forming the
DEVELOPMENTAL GYNAECOLOGY
ovarian medulla. Unlike the male, the surface epithelium continues to proliferate.
A second generation of cords are subsequently formed known as the cortical
cords. In the fourth month, these cords are split into isolated clusters each
surrounding at least one primitive germ cell. The germ cells then develop into
oogonia and the surrounding epithelial cells become the follicular cells.
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1.2.2
Abnormal development
Mllerian anomalies
Numerous abnormalities have been described, many with no clinical
relevance and others with profound importance. The incidence is
approximately 0.5% of the population, with a higher incidence in those
patients with infertility. The American Fertility Society classification is most
commonly used. This classification includes the following anomalies:
hypoplasia/agenesis
unicornuate
didelphys
bicornuate
septate
arcuate
diethylstilboestrol related
Aetiology and presentation
The cause of Mllerian anomalies is unknown. It is assumed that
abnormalities in the development of the paramesonephric ducts are
responsible. This may be due to non-development of one or both ducts
or non-canalisation. Seventy-five percent of women with anomalies will be
asymptomatic and other presenting symptoms are summarised in Table 1.4.
Secondary sexual characteristics are not affected as ovarian development is
usually normal.
Symptoms
Clinical presentation
Primary amenorrhoea
Pelvic mass:
Haematocolpos/haematometra
Ectopic pregnancy
Menorrhagia
Obstetric complications:
Uterine rupture
Malpresentation/abnormal lie
Preterm birth
Infertility/recurrent miscarriage
Endometriosis
DEVELOPMENTAL GYNAECOLOGY
Management
Appropriate and sensitive questioning, examination and counselling
are often required, as are investigation with ultrasound, MRI and
hysterosalpingograms. More invasive investigation with hysteroscopy and
laparoscopy are often indicated too. Due to the association of genital with
urinary tract malformations the use of intravenous pyelograms is warranted.
The management of these anomalies is dependent on the actual anatomical
abnormality and its significance. An imperforate hymen may present in
neonatal life with a mucocolpos or at puberty with cyclical pain and the
presence of a purple-blue bulge at the introitus. Presentation at puberty
may be accompanied by cyclical abdominal pain and primary amenorrhoea
prior to referral to the gynaecologist. Treatment is simple and effective by
performing a cruciate incision and thus allowing drainage and flow.
Any abnormality preventing efficient flow of menstruation should be corrected
to prevent the formation of endometriosis.
Vaginal septae can be removed surgically. It is prudent to remove the entirety
of the septum to prevent the formation of a stenotic ring that may lead to
dyspareunia. Occasionally a combined abdomino-perineal procedure is
required.
Uterine septae may be removed hysteroscopically and horns of a bicornuate
uterus may be joined together by an abdominal metroplasty.
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12
1.2.3
Intersexuality
Aetiology
Sexual development may be abnormal in the following circumstances:
46XX/46XY mosaicism
Anatomical/enzymatic testicular failure
Androgen insensitivity
Deficient MIS production
Excessive testosterone production in a female fetus (eg congenital
adrenal hyperplasia)
DEVELOPMENTAL GYNAECOLOGY
Presentation
Intersex may present in a variety of ways at different times of life depending
on the severity of associated symptoms (Table 1.5).
Neonate
Infant
Adolescence/adulthood
Ambiguous genitalia at
birth
Ambiguity of developing
genitalia
Salt-losing crisis
(congenital adrenal
hyperplasia)
Primary amenorrhoea
Delay in puberty
Sexual dysfunction
Infertility
Investigation
Initial investigation is dependent on presentation. Tests often required
include:
Karyotype
Testosterone, luteinising hormone and follicle-stimulating hormone, 17hydroxyprogesterone
Androstenedione, dihydrotestosterone, oestradiol
Human chorionic gonadotrophin (hCG) stimulation test
Synacthen test
Renal ultrasound
MRI
Management
An early and correct diagnosis is paramount. Unnecessary delay and
inaccurate diagnosis only confound the psychological trauma to the
individual or their parents. Involvement of a multidisciplinary team is essential.
This team should consist of an endocrinologist, psychologist, gynaecologist
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14
DEVELOPMENTAL GYNAECOLOGY
True hermaphroditism
Rare in Europe and USA, a higher prevalence is seen in Africa. The gonads
may be a varying mix of testis and ovary. They present with differing degrees
of sexual ambiguity. The degree of masculinisation is thought to be due to the
proportion of testicular tissue. The karyotype is commonly 46XX, with some
having a mosaic XX/XY and fewer having 46XY. Gender assignment may be
difficult and should be ascertained on an individual basis. Eighty percent
have female organs and are potentially fertile.
1.2.4
Karyotypic abnormalities
Turner syndrome
This is the commonest abnormality of women involving the sex
chromosomes. The majority of pregnancies with this karyotype are usually
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16
Physical anomalies
Webbed neck
Cardiac defects/aortic
aneurysm
Primary amenorrhoea/
absent secondary sexual
characteristics/ovarian failure
Shield chest
Hypertension
Cubitus valgus
Diabetes (25%)
Hypothyroidism (30%)
Renal dysgenesis
Nail dysplasia
Osteoporosis
Eye deformities
Table 1.6: Presentation, physical anomalies and long-term complications of Turner
syndrome
DEVELOPMENTAL GYNAECOLOGY
1.2.5
Conclusion
&
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