Gineco ENGLISH

Licci, Laserra Lez.
I - Gynaecology and Obstetrics Prof Ambrosini, 01/10/19
Licci Giuseppe,
01/10/2019
Laserra Piergiorgio Alberico Gynecology, lez 1
Prof.
Ambrosini
GAMETOGENESIS, FERTILIZATION, OVARIAN

CYCLE
The professor explains that for a few years the course is short, in a month and a half we will do
everything. With two lessons per week, the last lesson should be on November 16th. So on some topics we
will not dwell as we should, but the professor is available for any questions or clarifications.
Gynaecology and obstetrics is a wonderful branch that involves multiple fields: there is the biological
part, the pathophysiology of reproduction, medically assisted procreation, the radiological part understood
as ultrasound, oncology, delivery room and obstetrics, some surgical interventions such as cesarean
section, vaginal section. It is a branch that can satisfy a doctor's ambitions both from a surgical, medical
and scientific research point of view. They've never been able to break gynaecology down into different
medical specialties. Perhaps it's the biggest specialty of all.
This lesson on gametogenesis and fertilization is not much fun for a gynaecologist who actually deals
with patients every day: gynaecology is a practical branch, you have to treat patients and solve their
problems. This part, on the other hand, is more laboratoristic, more embryological, but it is also true that
this is where we begin: if there were no fertilization, gynecology would not exist, but neither would we.
Once the two gametes meet, an event that is all about gynecology begins: pregnancy. This is an event
that leads to the birth of the fetus through fertilisation (i.e. with the meeting of the spermatozoon and
oocyte) and which then takes place with the birth, i.e. the
exit of the fetus from a woman's body, either through the
vagina or through the abdomen with a caesarean section.
The pregnancy lasts 40 weeks. We doctors reason for
weeks, not months, also because the obstetric rule is
made on the weeks as well as the appointments
(ultrasound or other examinations).
When we say 40 weeks it means that by convention we
always start counting from the last menstruation, which
we mark on the ruler, and 40 weeks later technically the
baby should come out. Any woman ovulates about
halfway through her cycle (between 12 and 16 days if
the cycle is regular), the baby then actually comes out
when she is 38 weeks old. This reasoning is made,
however, on who is a clock, ovulation is not so regular:
some can ovulate first, others in 20 days.
The embryo, which is the product of conception, is called a fetus after 12 weeks. When it's born, it's
called a newborn.
The fetal annexes are all the stuff we get once we get the baby out. Amniotic fluid comes out, umbilical
cord, placenta. The placenta is the nutritive metabolic exchange organ between mother and child that will
have through this everything they need (oxygen, proteins, sugars, etc.).
Obstetrics rule
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Licci, Laserra Lez. I - Gynaecology and Obstetrics Prof Ambrosini, 01/10/19
This wheel is in every gynaecologist's pocket. The red arrow indicates the first day of your last period.
When the arrow marks the day the patient says, the other arrow automatically estimates when the baby
should be born. Every time the patient comes to visit I can know exactly what week the patient is visiting
and this will allow us to know exactly what to do.
The fetus and the newborn are actually quite the same: the first is a really fully formed baby, it will be a
miniature baby to all intents and purposes. The embryo on the other hand is different, it looks like a small
bean with a caudal and a cranial area.
Images of placenta, umbilical cord and

fetal membranes flow. Amniotic fluid is
all that comes out once the baby comes
out.
Fertilization can be:
 natural, with a group of
spermatozoa starting to move up
to the distal portion of the tubes
where only one fertilizes the
oocyte and the fertilization
product returns to the uterus after
4 days,
 artificial, in which with a needle
eight times thinner than a hair we
puncture the oocyte by injecting
the contents of a spermatozoon
we like. Afterwards, the embryo is grown 5 days and the implantation is attempted in utero.
Regardless of how the fertilization took place, in any case the embryo must be implanted in the uterus and
it is important that there is mitosis for cell duplication and meiosis for the division of the genetic heritage
into the 23 chromosomes.
In fact, while the spermatozoon is haploid (23 chromosomes), the oocyte has a diploid heritage (46
chromosomes). The egg must therefore halve its chromosomal count in order to meet the spermatozoon.
While the man has XY sex chromosomes, the woman is XX. The spermatozoon can contain an X or a Y,
the egg has two 23X and will have to become haploid to meet daddy's trousseau.
It will be the case to choose which chromosome of the pair of homologues will hold the egg cell.
Woman in the fetal stage produces primary diploid oocytes. With ovulation the first meiotic division is
completed and the secondary oocyte is formed, which is what will be fertilized. This will stay still in
metaphase II until the fertilization and only after the fertilization will complete the meiosis].
Therefore, spermatogenesis and ovogenesis have differences. The egg is a ball and a ball remains, but
spermatogenesis causes a round cell (primary spermatocyte) to pass from a round cell (primary
spermatocyte) to spermatozoa with a
different shape, with a halved
chromosomal patrimony. You go from
primary spermatocyte to spermatozoa.
The head becomes small, the neck
develops and will be the engine with the
mitochondria, the tail will have the
assonemas that allow to move. This cell is
not like all the others we have, it's
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incredible and it can move. If it didn't have this particular shape the sperm would remain in the vagina
and would not fertilize.
Male and female gametes must be different, one has the ability to penetrate and give rise to life, the other
has the ability to move and penetrate. This is the only way natural fertilization is possible, otherwise I can
only fertilize in the laboratory.
Sex cells during gametogenesis multiply through a meiotic process that involves double cell
multiplication with a single DNA duplication, so that from one mother cell 4 daughter cells are formed,
each with half a chromosomal kit.
The oocyte has many layers, for example we have the

follicular cells with the oophore heap, but we will be of
little interest if we do not take care of the assisted
reproduction part. "Little will interest you in the sixth
year of medicine to know all these things, there will be
other important notions of practical medicine (for
example to understand things like endometriosis,
childbirth, placenta previa)".
The egg is extruded from the ovary at the moment of

ovulation and is picked up by the fimbrias of one of the
two tubes. Let's imagine that the uterus is a goalkeeper,
the tubes are the arms and these arms are very good because they have a chemotacticism, so as hands both
move towards the egg. If this is extruded from the left, the right tube also moves to the left at the time of
ovulation. At this point the oocyte enters the distal portion of the tuba and will meet the spermatozoa that
from the vagina have reached the tuba, if there has been fertilization the embryo must move into the
uterine cavity and must find the right place to penetrate the endometrium with a small placenta species to
attach the plug and be able to continue living. Otherwise, after 4-5 days the autonomy ends and the
embryo dies.
Why might the egg not come this far?

 the sperm can't fertilize it.
 the tubes don't do their job and they don't carry it to the uterus. Maybe they don't have a
functioning ciliate mucosa.
The human being has only one fertilizable egg every month. The follicle-stimulating hormone of the
pituitary gland acts on specific receptors on the granulosa cells of the primary follicles, both on the right
and left ovaries. Then a dominant follicle grows, everyone else goes into atresia. It can rarely happen that
a couple of them grow up, but no more than many. In fact, most of us make one baby at a time.
We also know stories of births with more children, but there we have to understand if there were three
eggs fertilized by three sperm (the situation of fraternal twins is particularly difficult if not by in vitro
fertilization), or if one fertilized egg split in the first days, easier in natural fertilization. All the pushchairs
that we see today with two children and that were not so frequent before are related to assisted
reproduction.
The spermatozoon is a Formula 1 machine. The

head is small, it moves very fast, it is light but
has all the chromosomal heritage. On the tip of
the head it has lytic enzymes (hyaluronidase and
acrosine) to enter the oocyte via the oophore
heap and the zona pellucida. It has a neck for
3X
energy with mitochondria and a very powerful tail with various assonemas to move very fast. Without the
sperm we couldn't be here.
Certainly in the past it has helped a lot that a man could fertilize more women, for reasons of survival. It
is not necessarily that a relationship leads to fertilisation, just as it is not necessarily that the embryo is
born, that the child survives for a long time. Today the world is different, we have medicines, the right
food, heating. We'll get to be who knows how many in the world, but fortunately for us the human race is
not very fertile. Even a full report gives us little chance of having a baby in our arms.
How long does it take a spermatogonium to become such a specialized cell? 72 days, plus about ten days
of maturation in the epididymis to be ready to fertilize. About three months in all. If I take a drug that in
some way can alter sperm production (for example an antibiotic), this will produce visible effects on the
spermiogram in three months, not today. The sperm that ejaculate today is already well prepared.
In the epididymis, spermatozoa complete maturation and acquire motility. Man produces sperm all the
time.
The mature spermatozoon guided by Sertoli and Leydig cells then reaches the level of the epididymis
where it acquires a sperm coat, a secretion of the seminal vesicles and prostate which is also used for
immunological tolerance.
When they finish their total maturation, the spermatozoa do not come out on their own, but with seminal
plasma: fluid produced by Cowper's bulbourethral cells, seminal vesicles and prostate.
This liquid is used to carry out the spermatozoa, but also to form the sperm coat that protects them in
areas of the vagina, for example, from the pH and the unfavourable immunological environment. The
semen comes out coagulated and after a while becomes liquid; when it dissolves, the sperm lose this
protection and begin to run, but many of them die. Only a few spermatozoa reach the bottom, because the
vaginal environment is hostile, even the cervical mucus could be hostile depending on the woman, age,
infections and many other variables.
At a certain point there is the removal of the sperm

coat (also thanks to the movement of the spermatozoon
which, so to speak, is "cleaned"), which allows the
capacitation, the phenomenon for which at that
moment the spermatozoon is capable of fertilizing.
Exactly consists of an increase in membrane
permeability of the sperm for about 5-6 hours. So
there's not much time to fertilise and 99% of the sperm
don't pass. This obviously happens with a normal
ejaculate, if the ejaculate has problems the fertilization
becomes even more difficult.
Acrosomial ration
When the sperm head rests on the oophore
heap that protects the oocyte, the
hyaluronidase enzyme allows it to pass.
Then the acrosine will bind into the plasma
membrane and the sperm throws its contents
into the egg cell. Once penetrated, the egg
depolarizes its membrane and will not allow
other sperm to enter. We talk about
hardening zone: the zona pellucida becomes
hard and can no longer be penetrated.
4X
At this point we have the completion of meiosis, the union of the two pronuclei and the mitotic division
of the zygote. It starts from the blastomeric stage (4-8 cells), up to the morula, with many more cells,
which replicates with great speed and has the capacity to implant itself. The implantation takes place
more or less in the sixth day and the embryo is called blastocyst, because it has like a cyst, a cavity.
The blastocyst has enormous potential to penetrate the endometrium and find a space to insert itself,
through the chorionic villi it nests and takes the blood from the mother to supply itself with everything it
needs to grow. But this can only happen if the endometrium is in the so-called implant window: it must be
perfect for the spongy area, the number of capillaries and glands.
How do we know if a person is pregnant? She's not getting her period. Some people understand this
because they feel a bit strange, but the best way is to look for the beta fraction of HCG, the hormone that
the trophoblast produces. This hormone creates a series of symptoms in women, it's like a poison.
The nesting is nothing more than the

mechanical adhesion to the uterine wall and the
connection with the maternal circulatory
system. The endometrium must be in the initial
secretive phase which normally occurs after
ovulation, when the progesterone of the corpus
luteum arrives and begins to change the
endometrium into a secretive form
(endometrium full of vessels and glands). If the
endometrium is in another stage, it will not be
possible to have a pregnancy, although there
are rare cases in which babies are also formed
on the liver or in other areas. In fact, if the
blastocyst is very high quality, theoretically it is able to dig even in a wooden table, it is extremely
aggressive, but it must find some pots to grow, otherwise the embryo does not live beyond 6-7 days.
With nesting the deciduous is formed by endometrial reaction, mediated by estrogen progesterone on
embryonic stimulus. I have the proliferation of fibroblastic cells and the appearance of vacuoles with
glycogen and lipids.
This is when we can find beta-HGC in maternal vessels, after the trophoblast has encountered them.
That's why you have to wait 7-8 days for a positive pregnancy test, the basic test is done after 10-12 days.
Parallel to the formation of a uterus-placental circulation, the embryo begins to grow with three
embryonic leaflets (mesoderm, endoderm, ectoderm), each of which forms specific structures and
apparatuses.
If you stop growing right now, I have a positive pregnancy test and nothing more (biochemical
pregnancy). If the process continues and stops later we will talk about abortion.
In this image you can see the three sheets that
start to fold, obviously there will be a caudal
portion and a cranial portion. There's flexion
and then organogenesis. And a kind of flexed
bean is exactly what we see on the ultrasound:
at that point we know that organogenesis is
taking place.
Each one of these sheets produces tissue. For
example, skin and neurons are derived from the
5X
ectoderm, muscles and red blood cells from the mesoderm. This is something we can read, but with
gynaecology there is a lot but also little to do.
Eventually we'll have a cranial and a caudal area. From the umbilical cord will come the blood drawn
from the placenta which is well inserted into the maternal blood through digitiform formations.
The embryo then develops an external form, but also inside I have a differentiation in the various tissues
and organs.
The cardiovascular system is one of the things you see before. Seventh week I should see the heart at the
echo. Actually it may be visible from the fifth week: surely the earlier I see it (hopefully in the sixth,
unlikely in the fifth week), the more likely it is that the embryo is growing well (we speak of a positive
prognostic sign). I cannot tell the parents that I will see the heart before an echo in the fifth week,
otherwise I can alarm them; I will simply say that I will see a gestational chamber, a calf sac, an embryo
and that I probably won't see the heart because it is too early. I have to give the embryo time to grow. If,
however, at 7 weeks the measures are not normal and there is no heart that is an internal abortion, it is an
internal abortion to be rechecked in case of absence of heart but normal measures.
The professor reiterates the futility of explaining organogenesis in detail from embryonic leaflets.
Feto
The fetal development is such that it is not possible to be sure, until the moment of birth, that the fetus has
acquired all the functional capacities and a correct morphogenesis.
In fact, this must go towards the completion of morphogenesis of the palate, ear and external genitals, as
well as tissue differentiation. Proper development allows us to distinguish a healthy baby from a sick
baby.
During intrauterine development there is no direct measurement of the height and weight of the fetus.
Therefore, certain measures are used:
From week II to week XII, only the vertex-coccyx length is used.
After the 12th week, to get a better estimate of the size and weight of the fetus, additional measurements
are used, such as:
Distance between the two parietal bones
Head circumference
Abdominal circumference
Femur length
Length of humerus
We note how at week II the vertex-coccyx length is on average 1.55 mm, while at the end of pregnancy
it is between 30 and 35 cm.
6X
Immediately after delivery, newborn babies have an average height (vertex-foot plant) of between 48 and
52 cm.
Height and birth weight are not necessarily related to the weight and height that the newborn child will
reach once it has grown into adulthood.
[Teacher's clarification: when comparing two children in terms of weight and height it is necessary that
both are of the same gestational age. During the first month infants gain about 200 grams/week, so even
a single week of gestational age difference would make it impossible to compare the two babies].
Placenta
Definition: the placenta is an organ with a simple structure (exchange surface between the maternal and
fetal circulation) but with polyhedral and complex functions indispensable for the regular evolution of
pregnancy and the normal harmonious development of the fetus.
At the end of the pregnancy, the placenta appears as an oval disc with a diameter between 15 and 20 cm,
with a thickness of 2-3 cm. The weight is about 450-550 grams.
In the placenta one can recognize a dark red maternal face, formed by 10-38 (on average 16-18)
cotyledons (first order villi), and a pearly gray fetal face, covered by the amniotic membrane and from
which the umbilical funiculus departs.
Umbilical cord
7X
Inside the umbilical cord pass two arteries (umbilicals) and one vein (umbilical). Through an ultrasound
survey it is possible to identify these vascular structures which, in frontal section, will appear as three
circles.
If you notice the presence of only one artery, you should carefully monitor your pregnancy as this is an
alarm signal.
Maternal-fetal circulation
[the professor skips these slides, I'm just going to file them and bring them back in order, integrating
them with images to allow a better understanding, NdA]
Placental development:
Blastocyst plant
8X
Citotrophoblast
Invasion of the deciduous
Syndizotrophoblast formation of vascular gaps (Fig. 4)
Cytotrophoblast-deciduous connection (anchor villi)
Primary villi
Interval space
9X
Placental Development
Sinciziotrophoblast
Connection with maternal placental circulation vessels
Formation of the chorion internal surface trophoblast + extra-embryonic mesoderm
Secondary villi training
Chorionic Villas
Tertiary villi training
Equipped with a vascular component
Formation of fetal-placental circulation
The fetal-placental circulation is

such that there is no direct contact
between maternal blood and fetal
blood. The substances are carried
from mother to child through
blood-filled gaps.
10X
The placental fetal circulation consists of a maternal flow of 450-600 ml/min; the surface area of the
chorionic villi is about 10-12 m2.
For the fetus, the placenta performs the functions that in the adult individual are performed by:
Gastrointestinal tract
Respiratory system
Liver
Kidneys
and in addition the placenta performs irreplaceable endocrine, metabolic, immunological, enzymatic and
energy storage (glycogen) functions.
Hormonal changes during pregnancy
11X
Note that there is a much higher concentration of steroid hormones in term pregnant women than in non-
pregnant women.
The change in the hormonal profile means that pregnant women benefit from the positive effects of
oestrogen; among these, the most visible are the improvement of the skin and its appendages.
Another typical feature of the pregnant woman is the
increase in libido.
Also, the placenta produces non-steroidal hormones,
including:
HCG
HPL
CRH
cTRH
GHRH
NPY
Inhibin and Activin
ANP
Among the various placental functions, the most important to ensure a normal and harmonious
intrauterine growth of the fetus is certainly the transplacental passage of oxygen, since oxygen is the
essential comburent for the metabolic needs of the fetus.
12X
Note in the picture how only a few drugs can pass through the placental barrier and therefore only some
of them pose a danger to the fetus and its development.
Some pathogens also have a chance to pass through this barrier. These include CMV and toxoplasma.
Usually, in
the case of a planned pregnancy, anti-toxoplasma antibodies are measured for IgG and IgM.
If during pregnancy planning the mother is IgG positive no subsequent control for toxoplasma
If during pregnancy planning the mother is IgM positive resolution of the infection before conception
If the mother has no anti-toxoplasma antibodies during pregnancy planning, a monitoring programme is
followed to detect the appearance of antibodies.
The same screening model is also followed with other potentially teratogenic pathogens. The mother is
also urged to follow a lifestyle that limits the possibility of infection.
It should also be considered that any pathogen will have a stronger impact on the development of the
embryo or foetus as soon as contact occurs during intrauterine development.
Some antibodies can pass through the placental barrier, which can also pass to the newborn during
lactation. Therefore, the mother, both during intrauterine development and in the early stages of life, gives
immunological protection to her child.
Umbilical cord
13X
Wharton gelatine is a sort of sleeve that provides a mechanical defense of the umbilical cord content and
prevents it (in principle) from being crushed when the cord is twisted around the neck or around the
scapular cingulate of the fetus.
Fetal membranes
Time of childbirth
14X
In figure the event of childbirth

During this moment it is possible to notice all the complicated changes of position that the fetus has to
take in order to exit through the vagina.
In order to ensure the correct release of the child and the health of the mother, various devices and
methods of investigation are used. In particular:
Assessment of the position of the fetus within the uterus
Assessment of the presence and frequency of uterine contractions
Assessment of cervical dilatation
Fetal heart rate monitoring equipment
During a natural childbirth the mother loses a considerable amount of blood, either due to traumatic
factors depending exclusively on the passage of the baby through the vaginal canal, or due to obstetric
maneuvers.
In the period just before the birth it is noted that the mother is characterized by a profile of
hypercoagulability; evolutionistically this mechanism has remained to allow the mother to give birth
without losing excessive amounts of blood. Despite this adaptive system, today you can take advantage of
surgical techniques to further reduce blood loss by the mother.
OVARIAN AND MENSTRUAL CYCLE

Definitions:
Ovarian cycle: monthly cyclical changes to the ovary
15X
Menstrual cycle: monthly cyclic changes to the endometrium
Pituitary hormones
The hormones produced at the pituitary level are gonadotropins, LH (luteinizing hormone) and FSH
(follicle stimulating hormone).
The biological activity of gonadotropins is different depending on the period of an individual's life.
 During the prepubertal phase there is low biological activity due to the higher acidity of the
molecule;
 During puberty and after menopause there is a higher biological activity of these hormones due to
the pH change of the molecule towards more basic values.
At different stages of an individual's life there will also be variations in the concentration of
gonadotropins:
 Low during childhood;
 During puberty there will be a pulsatile increase in concentration (mostly during sleep);
 In the postpubertal era the levels will become more regular again;
 In menopause there will be high levels again.
Gonadotropin secretion is pulsatile. In particular:
LH has a peak concentration every 60-80 minutes during the follicular phase (first phase of the cycle) and
every 100 minutes in the lutein phase (second phase of the cycle).
FSH has small variations in concentration and a long half-life.
[Professor's digression: If a girl under the age of 13 years (e.g.: 9 years) has already reached puberty
(stage of sexual development characterized by the appearance of hair and secondary sexual
characteristics) and telartric (development of the mammary glands and therefore the breast), it may be
necessary to intervene to reduce the secretion of gonadotropins and postpone the start of maturation of
the girl. ]
Ovarian hormones
The ovary is the main endocrine gland responsible for the production of sex steroids; the cells responsible
for the production of these hormones are the cells of the granulosa, stromal and interstitial.
16X
All sex hormones have a common starting chemical structure to which are added chemical groups that
involve their different function and activity. These hormones are produced mostly at the gonadal level, to
a lesser extent at the adrenal level and, during pregnancy, also by the placenta.
The professor skips a few slides I'll insert below for completeness.
Estrogens
Estrogens are a group of sex hormones including estradiol, estrone and estriol.
Estradiol is the main estrogen, synthesized at follicular level mainly by granulose cells (as well as techal
cells), through a process of aromatization (reaction mediated by the aromatase enzyme) from androgens.
The medium estradiol induction of enzymatic pathways (metabolic effect) and proliferation of target cells
(mitogenic effect).
Estrogen is the main estrogen during menopause. Its biosynthesis can take place thanks to the
dehydrogenation of oestradiol and the aromatization of androstenedione. There is a percentage of extrone
(10-15% of the total) that is produced in locations other than the ovary. These include adipose tissue,
skin, CNS and liver.
The professor says the estriol is of little

importance, I'll report the slide for
completeness.
[Professor's Disquisition: Given the
possibility of extraovarian oestrogen
production especially in adipose tissue,
women above the obesity threshold are at
17X
greater risk (for the same genetic risk, see BRCA1 and BRCA2 mutations) of developing hormone-
sensitive breast, ovarian or uterine cancer.
Current Italian society is going against a considerable increase in menopausal women. This depends on
the fact that between '65 and '75 of the last century there was a boom in births given the economic
prosperity into which Italy poured. The group of people born during these years is otherwise called
"Baby Boomers". This group of people, and particularly women, have now reached the age of
menopause; having been many births in those years then there are now many women in menopause, more
than there were in previous years.
In 2000, a study (WHI - Women's Health Initiative) was published to demonstrate the effectiveness of
hormone replacement therapy during menopause. Preliminary studies showed that this therapy could
slightly increase the risk of developing hormone-dependent neoplasms. The media swelled this news a lot,
based only on preliminary studies and for a long time very few women have benefited from this therapy.
Fortunately, through a work of re-qualification of study and popular knowledge, the number of women in
therapy has increased significantly]
Progesterone and androgens
Again, the professor skips a few slides; I'll report them below for completeness.
18X
Gonadotropin secretion
19X
The professor keeps skipping slides and reading some of them; I'll report those slides below.
20X
Casarotto Arianna 03-10-2019

Zilio Matthias
Gynaecology, Lesson No. 2
Prof.
Ambrosini
OVARIAN CYCLE AND MATERNAL CHANGES IN PREGNANCY

ENDOCRINOLOGY OF THE OVARY
As far as gametes are concerned, it is important to know that what differentiates us from other species and that
it is also the difference between man and woman is precisely the fact that the man can produce the male
gamete until late age, some perhaps even until old age, while the woman is born with a predetermined oocyte
heritage that she loses continuously throughout her life. The woman around the age of 45-55 will no longer
have eggs and will therefore definitely go into menopause.
OOCYTE
The oocyte heritage is determined during fetal life and depends on the primordial follicles that are ready to
mature and grow and then be stimulated by the FSH hormone that will make them grow again and allow some
follicles to become a follicle that will lead to the production of a normal, mature egg ready to be fertilized.
21X
In fetal age, there are about 6 million eggs inside the small ovaries of the baby; in puberty, when the cycle
arrives, therefore, when the woman will become fertile, there are 4000 eggs. If the woman ovulated 10-12
times a year and did it for 40 years, 400 eggs would be enough. The problem is that every month a group of
eggs grows and only one becomes the egg that will be extruded and that can be fertilized or not, while the rest
will go to atresia and die. Therefore, every month there is a loss of follicular assets. In addition, over time, the
follicular heritage of these unreplicating cells loses its quality because it is damaged by free radicals, like the
damage that any other organ has suffered for a long time. It is easier to see the damage of time on the hair, skin
and body; while it is difficult to see the damage of time on an ovary or liver.
DEVELOPMENT OF PRIMARY FOLLICLES
The ovary has the ability to develop the primary follicles, visible in
the image. The primary follicles must mature, develop the cells of the
granulosa and continue the development, or in those follicles where
this does not happen they subsequently go into atresia, and in this case
we speak of an unfinished cycle. All these small primary follicles have
to become competent to grow, but after they are grown they could go
to atresia, because only one will have the chance to become big.
In the image on the right, a follicle is represented which consists of:
- An oocyte;
- A cavity filled with liquid
On ultrasound, the follicles are clearly visible due to the
presence of the hypoecogenic liquid, otherwise their
localization would be extremely difficult;
- The oophore heap that envelops the oocyte;
- The zona pellucida
- The cells in the case and the granulosa necessary for the
production of hormones.
The menarche is the first day of menstruation, appears in most

girls around the age of 12-14 years and indicates that the ovary has
begun to function, so it is an indication that the gonadostat, a part
of the brain, has begun to give input to the pituitary gland to
function which in turn gives the stimulus to the ovary to grow eggs,
while ovarian hormones give input to the endometrium to grow and
deshalate and consequently to have menstruation. The menarche
should appear within a normal age range otherwise it could be
worrying.
In the initial recruitment, hundreds of follicles are recruited, and

the cells of the granulosa multiply and form the primary follicle.
After three cycles, the cells in the inner casket will form. This forms the secondary or pre-anthral follicle.
Only the follicles that become pre-anthral are follicles that can be stimulated by gonadotropins and
consequently grow. There are many primary follicles that mature, the granulosa cells multiply and the
secondary follicles that form are those that have the ability, thanks to the input from gonadotropins, to grow.
The primary follicle differs from the secondary follicle: the primaio follicle is a whole cell without liquid
inside it, so it will be absolutely invisible to the sonographer's eye; while the secondary follicle has a small
cavity that becomes visible. Thanks to the ultrasound you can do an antral follicular count. In the first days of
the cycle, in the 2nd-3rd day, it is used to evaluate the capacity of the ovary and is used to see how many
theoretical eggs a woman has. It will be normal to find many eggs in a young woman and few in a woman of a
certain age. Particularly important is the evaluation of antral follicular count in sterile women, who have
difficulty having children, because pre-antral follicles, i.e. those follicles that can be stimulated, are evaluated.
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Counting allows you to understand the dosage of drug to be used and the type of response that the patient will
have with medically assisted procreation and therefore know the reproductive chances. For example, if a
woman has one ovary with 10 small follicles, there is hope that 10 follicles can grow; if the ovary has 1
follicle, there is hope that only 1 follicle can grow. This is a predictive figure, but for a pregnancy other factors
also count, including the age of the patient, the other genitals, the husband's semen and much more.
After two cycles, there is the formation of the cavern and

the formation of the external shrine then there is the
formation of the tertiary or antral follicle. At this point, you
will have a follicle size of 5-8 mm which represents that
follicle that can become the dominant one. All follicles
begin to grow, but when one becomes particularly large it
is called a De Graaf follicle. De Graaf's follicle develops
the oophore heap around the oocyte, is larger in size and is
the only one that responds to the stimulus of
gonadotropins, while in the remaining follicles the
receptors for them disappear.
Summing up, at each cycle you already have a lower
number of eggs than at the start, some eggs die from
apoptosis due to time, others grow and try to become a
follicle under the stimulus of gonadotropins but fail, only
one becomes the De Graaf follicle; all this leads to a
further loss of follicles every month. The problems of
sterility or old age were not present 40-50 years ago
because it was customary to look for children at a young age.
STEROIDOGENESIS
The ovary produces estrogen, progesterone and androgens, which are also produced by the adrenals. The
whole chain part of cholesterol. The pregnenolone pathway makes it possible to have androstenedione which,
thanks to the enzyme 17-alpha-reductase, produces testosterone and by aromatization produces estrone and
estradiol.
FSH and LH
The prince egg stimulator is always the FSH. FSH stimulates the cells in the granulose to produce estrogen by
giving a mitogenic effect that allows them to produce estrogen, increase gap-junctions, and kill the receptors
for LH, the luteinizing hormone, which stimulates the production of progesterone. LH also has another
function: blocking mitosis. The action of this hormone prevails in the second part of the cycle, LH blocks
mitosis and causes a growth blockage of some follicles that consequently cannot become dominant. In
addition, it stimulates steroidogenesis for progesterone and activates plasminogen for ovulation.
EXTRADIOL
Estradiol is in great synergy with FSH, they communicate through feedback thanks to blood dosages. Estradiol
allows the receptors for FSH and LH to leak.
High levels of FSH allow important follicular growth and estrogen production. Low levels of FSH, do the
opposite: there will be a decrease in thrust towards follicular growth and therefore follicular atresia.
PROGESTERONE
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Progesterone is produced by the corpus luteum, the follicle envelope; it is produced after ovulation, therefore
in the second part of the cycle, in particular 7 days after ovulation, from this moment it will be possible to dose
it. Progesterone has the ability to block follicular growth by antagonizing FSH.
MESTRUCTION
Menstruation is a visible event. Menstruation is a bleeding through the vagina coming from the uterus, it is
cyclic and this indicates that someone has stimulated the endometrium to grow and as a result the ovarian
hormones responsible for the growth of the endometrium have been produced and the ovary has worked. The
menstruation appears 14 +/- 2 days after ovulation. The cycle occurs after 28 days, it is considered normal
even if it occurs after 26 or 30 days. Whereas if the woman had her period before 26 or after 30 days, she
should be studied.
The post-ovulatory phase is constant. This means that not all women ovulate in 14 days, but if they ovulate,
after 14 days you should have your period.
At the beginning of the cycle some follicles

are able to respond to FSH because they are
the ones that express the highest number of
FSH receptors. FSH stimulates follicular
development and stimulates the granulosa cell
to produce estrogen. Initially there is a modest
increase in estrogen. In the first phase of the
cycle, 7-8 days after the onset of FSH
stimulation, there is a significant increase in
estrogen as shown in the graph opposite. The
more estrogen increases, the more receptors
for FSH on the granulose cells increase and as
a result there is a further increase in estrogen.
The follicle that will produce the most
estrogen will be the dominated follicle.
The maximum estrogen production will be

before ovulation and in any woman. 99.9% of women produce a single follicle capable of bursting and
extruding the oocyte and have the estrogen peak before ovulation within a range of picograms of estrogen that
is always the same. The case of in vitro fertilization is different. In in vitro fertilization, FSH is administered
continuously, so not only a dominant follicle grows, but also all the others that therefore will not go into
atresia. Since the mechanism is identical and the production of estrogen is the same, there will be no
physiological estrogen dosage in this situation. If blood tests are performed, the dosage will be much higher.
FOLLICULAR SELECTION
Follicular selection is normally a physiological cycle. It is characterized by high levels of FSH stimulating the
production of LH receptors in the case and a response to LH produced by the pituitary gland. LH, once bound
to receptors, increases the production of progesterone, androgens, delta-4-androstenedione and testosterone.
High levels of FSH stimulate the granulose cells to produce estrogen which can then be aromatized.
The selection of a follicle that increases in volume compared to the others will always be present at each cycle;
this is responsible for the production of most estrogen and is the one who should extrude the best oocyte that
will have to be captured by the fimbrias, go into the tubes where it will meet a spermatozoon.
The selection of the dominant follicle is evident from the first days of the cycle. In the first days of the cycle
we observe the follicles that are recruited and that can grow: the follicles that will grow will have a diameter of
5-8 mm. If there was a larger one it means that it is a cyst; while other smaller formations will not grow. If
among the 5-8 mm follicles, one is 7-8 mm it is very likely to be De Graaf's follicle. In addition to the
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diameter, other requirements are the presence of numerous granulosa cells and the ability to concentrate FSH
and estradiol (E2) within the follicular fluid preventing androgen-mediated atresia.
In the selection of the dominant follicle, there will be a peak of FSH which is very short and very fast which
will benefit De Graaf's follicle, the others will go into atresia.
There will be secretions of the dominant follicle of FSH-inhibiting factors: inhibin, follistatin and estradiol. At
some point FSH production is inhibited.
OVULATION
Ovulation is linked to a rapid increase in estrogen (estrogen peak) and LH (LH peak) levels. 36 hours after the
LH peak, there will be a chance to ovulate: the follicle will burst and the corpus luteum will form from the
follicle envelope. The oocyte will be extruded and captured by the tuba and if the oocyte is fertilized by the
spermatozoon the corpus luteum will become a pregnant corpus luteum.
OVULATION MECHANISM
The mechanism of ovulation is a bit peculiar and we don't really know exactly how it happens. Ovulation is
known to respond to the LH peak: it has been seen that 36 hours after the LH peak ovulation occurs. LH allows
a rapid increase in follicle volume, local hyperemia, protrusion of the follicle on the ovarian cortex, formation
of stigma on the follicular wall and rupture of the follicle with release of the mature oocyte. There is a
weakening of the follicular wall with dissociation of fibroblasts and techal cells, dissociation of the granulosa
cells, increased osmotic pressure in the follicular fluid, disintegration of the case and contraction of the smooth
muscle cells in the case.
FOLLICULAR ATRESIA
The other follicles, those initially recruited, which have started to grow but have not grown big enough, go into
atresia. Inside, in the follicular fluid, these follicles have high concentrations of androgens. These are follicles
for which there is a great growth of FSH inhibiting factors: inhibin, follistatin and estradiol. Therefore, they are
follicles that will no longer be able to be stimulated by FSH and will progressively reduce their volume and
then die. There's talk of granulosa cell death with follicle atresia.
LUTEAN BODY
The corpus luteum is represented by the "peel" of the follicle which is transformed into an endocrine organ: it
produces progesterone. The progesterone is fundamental for endometrial decidualization, the latter will be
ready to receive an embryo. The corpus luteum has a yellowish color due to cholesterol-related pigments.
It stands out:
- the menstrual corpus luteum, if menstruation will be present;
- the corpus luteum gravidarum if the patient remains pregnant. In pregnancy the corpus luteum
becomes very important because it will be able to produce a huge amount of progesterone needed
during the first three months of pregnancy.
The menstrual corpus luteum lasts 12-14 days; it has maximum activity 7-8 days after ovulation. If you want to
know if a patient produces the right concentration of progesterone, the examination should be performed 21
days after menstruation. In women where the corpus luteum does not work well and does not produce enough
progesterone you will have an endometrium that does not grow properly. Progesterone stimulates the glands
and vessels to grow as well as stimulating the growth of spongy tissue. In this way the endometrium takes on a
different histological and ultrasound aspect and is suitable for embryo rooting and consecutive pregnancy. If
the progesterone is missing this will not be possible and there will be a spotting effect, more present in late
age. Spotting is represented by small bleeds in the second phase of the cycle that may indicate the presence of
LPD (low progesterone disease), the low progesterone disease, linked to an unskilled corpus luteum.
Luteolysis occurs 2-3 days before menstruation. The formation of the corpus luteum blocks the development
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of other follicles. The corpus luteum is formed because the cells in the granulosa and the case become luteinic
and both secrete progesterone.
Low levels of LH are necessary for the corpus luteum: it is present in the second phase of the cycle just when
LH is lower. When LH decreases it means that the cycle is over, when FSH rises again it indicates the
beginning of a new proliferative phase. Once again FSH will stimulate the follicles, the follicles will grow,
these will produce estrogen that will promote the release of LH receptors. LH and FSH will both have an effect
on the cells in the case and the granulosa that will continue to produce estrogen, progesterone and androgens.
These hormones will give positive and negative feedback on the pituitary gland and hypothalamus for proper
homeostasis. If the inputs are not right because of a problem along this axis, you could have many problems:
bleeding during the first or second phase of the cycle, follicles growing but not ovulating (disovulatory
woman).
During pregnancy, the hCG produced by the trophoblast keeps the corpus luteum functioning, making it a
pregnant corpus luteum. In this way, the hCG supports the corpus luteum which consequently will not go into
atresia and will continue to produce progesterone.
ENDOMETRY
The endometrium represents that part of tissue

that grows every month in the uterus and then
eventually desphalates. The endometrium has
the capacity to grow because there are receptors
on the basal layer, which will always remain so,
that respond to sexual hormones. When the
endometrium desphases, pieces of tissue fall
off. The menstruation is blood with the presence
of clotted blood with small pieces of tissue
representing the glands, spongy tissue and the
rest. When these pieces fall, they decapitate the
vessels that bleed. Thanks to the mechanism of
normal coagulation these small jars close
quickly, this is also due to the contraction of the
uterus which allows a mechanical hemostasis.
You will have a loss of tissue and blood for 2 to
5 days.
The basal layer does not change and allows the
regeneration of the functional layer. The
superficial or functional layer contains the
superficial epithelium of the glands and the stromal tissue. It is affected by the action of steroids. The surface
or functional layer is bound to the compact surface layer and the deep spongy layer containing the glandular
perforations.
MENSTRUAL CYCLE
Regenerative phase
The regenerative phase is the post-menstruation phase and is the phase in which the endometrium is
regenerating. In the first days of the cycle, there is an initial reconstruction of the superficial epithelium with
glands with short, straight and small-calibre tubules before becoming larger and festooned.
Proliferative phase
It indicates that there is an increase in estrogen receptors caused by estrogen itself.
In the initial phase, there are glands with short tubules and few spiral arteries; in the intermediate phase there is
an increase in tubule size, stromal edema and an increase in spiral arteries.
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In the advanced stage, there are numerous mitoses, tortuous glands, glycogen content, numerous spiral arteries
reaching the surface epithelium and progesterone receptors. The latter will be important in the second phase
and will play an important role in continuously modifying the histological geometry of this fabric.
Secretive phase
The secretive phase is a phase that undergoes the action of progesterone, while it decreases the action of
estrogen.
In the initial phase, 2 days after ovulation, there will be a stop of mitosis and an increase in the tortuosity of the
glands.
In the intermediate phase, there will be an accentuation of the characteristics of the previous phase, the
glandular lumens will be full of eosinophilic material and a marked stromal edema will be present.
In the advanced stage, there will be a dilation of the glands, a decrease in stromal edema and the spiral arteries
will be well differentiated and evident.
All these phases are visible if you study the tissue on a corpse. Today, with ultrasound, it is possible to
understand whether the woman is in an initial proliferative or ovulatory phase or in an advanced or
intermediate or initial secretive phase.
Desquamative phase
The desquamative phase is related to the fall of sex hormones and luteolysis. There is degeneration of the
spiral arteries, with blood leaking from the cavity; there is also disintegration and desquamation of the
structures: tissue loss and endometrial flaking.
MATERNAL MODIFICATIONS DURING PREGNANCY
When we talk about pregnancy, it means that the oocyte has encountered the sperm and created the embryo
that took root in the endometrium.
The pregnant woman will have physiological changes in response:
- Hormonal modifications;
- Fetal growth;
- Necessary for the smooth running of the pregnancy.
Physiological adaptation to pregnancy involves:
- Genital system;
- Cardiovascular system;
- Emocoagulative system;
- Uropoietic apparatus;
- Gastrointestinal tract;
- Endocrine system;
- Cute and musculoskeletal system;
- Respiratory system.
WEIGHT
There is a significant weight gain during pregnancy, linked to the increase in the volume of the uterus, the
growth of the fetus and the mother's body which becomes oedematous due to an accumulation of fluid. A
pregnant woman has to gain 12-13kg to have a good chance of returning to her initial weight at the end of
pregnancy; all the extra weight, on the other hand, is extra fat which will be more difficult to dispose of.
Weight gain involves both thin and obese patients, who have to eat in the correct way in order not to gain too
much weight because in these patients the 15kg increase is much less visible than in a thin patient: in fact, most
of the time, obese patients tend to relax in eating, not seeing that they are getting fat, and therefore tend to gain
more weight carrying both aesthetic and health problems. Therefore, obese patients, due to symptoms such as
nausea or lack of appetite in the first trimester, are advised to take advantage of these first months to improve
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their diet and lifestyle and try to lose a few pounds (even 10-15kg in the first 3 months) to ensure that the
weight gain in the following months is exclusively due to pregnancy and not fat.
The weight gain is due to several factors: the fetus weighs 3-4kg at birth, the placenta 0.5kg, the amniotic fluid
1.5kg, the uterus 1kg, the increase in blood volume 1kg (there are about 1.5l of blood), the breast 1kg, the
extracellular fluid 1.5kg, fat and protein accumulation 2-4kg. In pregnancy, fat is more easily accumulated
because the metabolism drops during gestation and in addition the pregnant woman accumulates several
calories with food.
An obese pregnant woman and a very thin pregnant woman show on the ultrasound, in case the fetuses grow
well, measures that are superimposable. The difference is that in the obese patient you immediately see the
increase in belly, while in the anorexic or particularly thin patient the belly initially remains very small: the
thing that counts, however, are the ultrasound measurements and the fetal well-being, because the belly is
linked to the presence of fat.
METABOLISM
There is a generalised increase in all physiological processes, including respiratory rate and cardiac output. It
must also be remembered that the fetus, the placenta and the mother need about 2500kcal/day total, which are
not many considering also the fact that the pregnant woman does not make many movements. It is also good
that the pregnant woman does not lose muscle mass and does a minimum of activity, such as swimming or
walking, because the muscles consume calories faster.
FEMALE GENITAL APPARATUS
USEFUL
From the 12th week of pregnancy the uterus will no longer be contained within the small pelvis, at 20 weeks it
reaches the transverse umbilical and at the end of pregnancy (36-38 weeks) it reaches the eighth intercostal
space.
There is a progressive retention of water, hypertrophy and hyperplasia of myometrial cells which causes an
increase in the weight of the uterus due to this imbibition: in fact the uterus goes from 40-70g to 1200g. The
uterine walls thicken up to 20 weeks and then thin out to 5-7mm. From 10-12 weeks, a transition zone between
the cervix (fibrous tissue) and myometrium develops at the isthmus level. There is a progressive increase in
blood supply and the myometrium, mainly released, increases its contractile activity proceeding towards the
end of pregnancy. The uterine contractions can be like contractions that make the uterus hard, and in this case
they are not dangerous because the uterus is a muscular organ, or rapid and rhythmic contractions, perhaps
even painless, which give changes in the cervix and in this case it is recommended that the pregnant woman
goes to PS for a visit also in consideration of the week of gestation.
CERVICE
The cervix during pregnancy provides the closure and mechanical support of the uterine body to ensure that the
delivery reaches its end. It becomes progressively softer due to increased edema, vascularisation and
modification of connective and endocervical glands. The glands produce mucus to create a mechanical and
biological barrier, as mucus allows bacteria or other substances that could damage the uterus to enter the
uterus. The cervix modifies itself in labour in childbirth by releasing proteases from endocervical granulocytes
with consequent dissociation of collagen fibrils.
VAGINA
In the vagina of a pregnant woman there is an increase in vascularization and therefore the vulva will appear
oedematous and hyperemic. There is an increase in vaginal secretion, which will be viscous and whitish, which
is called pregnancy leukorrhoea; this whitish loss is completely different from that of a mycotic infection,
which will be whitish but of a different consistency. The tissues are soft and soaked to help stretch the canal.
The outbuildings are located at the top as the uterus rises; the vessels are dilated and congested.
MAMMELS
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The udders have increased volume and vascularisation, have glandular lobe hypertrophy, have a
hyperpigmented areola and a whitish-yellow liquid production from the early stages of gestation (although not
all pregnant women have these secretions).
CARDIOVASCULAR
There is an increase in the ejection volume from 60 to 85 ml, an increase in the heart rate up to 32 weeks
(so the pregnant woman is tachycardic) and an increase in the cardiac output: so the heart of a pregnant
woman gets bigger because she has to make more effort. Sometimes during pregnancy some cardiovascular
problems are postponed and will be followed by the cardiologist to see if they will pass with the end of the
pregnancy or if they will remain. Therefore, the jugular distension, slight declivity, increased valve closure
tone and aortic-pulmonary blowing, tachycardia are physiological in the pregnant woman.
Question: If a woman has more than one pregnancy, can she be more likely to have cardiovascular problems?
Answer: If the woman is hypertensive she should try to plan for pregnancy at a stage where blood pressure is
normal; if this is not possible pregnancy becomes at risk. Pregnant women cannot use all types of
antihypertensive drugs, and hypertension increases the risk of preterm delivery and thus increases fetal
mortality. Certainly all cardiovascular problems worsen during pregnancy the same problems are not good
for pregnancy.
There is a decrease in peripheral vascular resistance and a decrease in blood pressure of at least 10-
15mmHg: therefore all pregnant women will be hypotensive and finding hypertension is absolutely not good.
There's myocardial hypertrophy with a shift to the left of the heart to elevate the diaphragm.
HEMOCOAGULATIVE SYSTEM
The blood count of the pregnant woman will certainly be different from other people, for example she will
have a lower hemoglobin, white blood cells a little higher. There is a 25-50% increase in blood volume
(1200-1900ml) for an increase in plasma volume and erythrocyte mass: a physiological gravidarum
haemodilution is present for adequate organ perfusion and protection against postpartum haemorrhage. This
until 32 weeks, when the plasma volume remains stable and continues to increase erythrocyte mass. In addition
there is an increase in the factors of hepatic synthesis coagulation (fibrinogen, factors VII, VIII and X) and a
decrease in fibrinolysis to have a state of physiological hypercoagulability that allows protection from
postpartum hemorrhage.
There is an increase in plasma volume (30-40%), with an increase in plasma without modification of
erythrocytes: in fact, haemoglobin concentrations are lower and therefore there is a relative anaemia during
pregnancy. There is an increase in cardiac output with an increase in cardiac ejection. There is supine
hypotension due also to compression of the vena cava by the uterus (if the pregnant woman wants to sleep in
lateral decubitus she will have to do it from the left side just to avoid such compression), reduction of venous
return to the heart and hypotension.
GASTROINTESTINAL SYSTEM
There is nausea and vomiting which usually end around 13 weeks: during this period the obese can try to
change their diet. Hyperemesis occurs in 2/3 of pregnancies in the first trimester and is linked to the action of
chorionic gonadotropin (hCG) and stress: in the case of twin pregnancies hyperemesis is more frequent due to
the presence of more hCG.
Another phenomenon that affects pregnant women is constipation, which is linked to the action of
progesterone, which acts as a myorelaxant on the muscle fibres of the intestine and allows an increased
absorption of substances, and the volume of the uterus.
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The gums become oedematous and hyperemic with a tendency to bleed when pregnant women brush their
teeth; moreover, pregnant women tend to have many bruises. Pregnant women can undergo prophylactic and
dental treatment.
Sometimes increases the frequency of gastroesophageal reflux that causes stomach acidity and heartburn,
even for a more intense production of gastric juice. To buffer this acidity, the pregnant woman can eat toast or
stale bread.
There is a decrease in tone, motility and gastric emptying, so it is better to follow a simple food profile in
which the pregnant woman is advised to eat little but often (5-6 meals a day) and the most abundant lunch
should be breakfast while dinner should be done early enough to be digested.
After the third month there is a reduction in gastric acidity which leads to an improvement in any gastric ulcer.
There is also a myorelaxation of the cardias which can cause reflux esophagitis: this reflux can burn the vocal
cords and cause aphonia.
Of course not all pregnant women will have these problems: there will be some who will have no problems at
all, some who will have almost all and most will have some.
There is a decrease in tone and motility of the small and large intestine with slowing transit and constipation
and an increase in water resorption of 60% at the colic level. There can be a profound alteration of the
bacterial flora with consequent dysbiosis, constipation and abdominal swelling.
There may be a change in liver function indexes and a tendency for gallbladder gallstones to form due to
increased volume and reduced motility.
CARBOHYDRATES AND PANCREAS
In carbohydrate metabolism there is a supplementation of energy directly usable by the fetus and the structures
involved in lactation and an action of hypoglycemic hormones that cause gluconeogenesis with insulin
secretion and glucose intolerance that can lead to gestational diabetes.
There is a hyperplasia of β pancreatic cells that produce insulin: in the first trimester the fasting glycaemia
decreases, but in the second and third trimester the fetus' energy requirements increase and glycogenolysis
occurs; as pregnancy continues, maternal resistance to insulin increases and the production of insulin
antagonists increases. So in the first half of pregnancy hyperinsulinemia allows the intake of glucose by
hepatocytes and adipocytes and the synthesis of glycogen; in the second half of pregnancy there is the
blockage of the insulin response with an increase in glucose levels that can be transferred to the fetus. The
glucose will then pass to the fetus which will become large and fat and may present the fetal macrosomy,
which is one of the most dangerous gynaecological aspects: in fact, in addition to having a large head it will
also have large shoulders and during delivery these may not be able to get out.
RESPIRATORY
There are frequent difficulties in breathing, especially at the end of pregnancy when there is a displacement
of the last ribs, a lifting of the diaphragm for the volume of the uterus and a decrease in pulmonary capacity.
There may be edema, hypersecretion of the nasal mucous membranes and hyperemia by estrogenic action;
there is elevation of the diaphragm with opening of the rib angle. There is an increase in the volume of air
exchanged at each respiratory act with hyperventilation, which will cause hypocapnia and consumption of
bicarbonates: respiratory alkalosis is compensated by metabolic acidosis.
URINARY SYSTEM
There is an increase in renal flow, an increase in glomerular filtrate with a modest tendency to urinary
retention, dilation of renal pelvis and ureters for a myorelaxant effect of progesterone and urethral compression
by the pregnant uterus (which can cause urinary stasis and urinary infections). There is also an increase in the
frequency of urination due to the volume of the uterus.
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There is an increase in renal plasma flow and glomerular filtration speed of 50-60% in the first two quarters
and 30% in the third quarter. There is increased clearance of creatinine, urea, uric acid, activation of the renin
angiotensin aldosterone system, hyperincretion of aldosterone. There is an increase in bladder pressure with a
decrease in bladder volume which leads to a demand for greater urethral continence: this causes a lengthening
of the urethra and an increase in closing pressure which can lead to stress urinary incontinence.
Changes caused by the pressure exerted by the pregnant uterus and the relaxing effect of progesterone on
smooth muscles,
increased renal
volume and dilation
of the pelvis,
pelvis and ureter
can lead to
ascending urinary
infections.
BRAIN
There is a
significant increase
in volume due to
progesterone, estrogen and prolactin: there will be an increase in volume and consistency from the first
weeks and hyperemia in the third trimester, when venous dilations can also be seen subcutaneously.
SKIN AND MUSCULOSKELETAL SYSTEM
There may be hyperpigmentation of the skin in 90% of pregnant women due to the presence of more
melatonin: therefore pregnant women in summer periods will have to protect themselves with 50 protection in
certain areas. In particular, the most affected areas on the face are the forehead, the temples and the cheeks
which may cause the "chloasma gravidica", whilst in the body are concerned the areoles, the armpits, the
genitals and the alba line, that is, those areas with the hairs where there is more melatonin and therefore
pigmentation.
Many pregnant women suffer from stretch marks (striae gravidarum) and the ligaments, especially the
sacroiliac joint and pubic symphysis become softer.
In the picture you can see how a woman's body changes during pregnancy: in particular you can see how the
belly increases more and more and goes upwards, while at the end of the pregnancy the belly lowers as the
fetus' head may already have reached the upper pelvic excavation and therefore leaves more room at the top.
Ruggero Lo Scalzo 08/10/2019

Erika Velotta Gynaecology, Lesson 3
Prof. Ambrosini
Pregnancy monitoring, obstetric and gynaecological ultrasound,

Abnormalities of pregnancy
PREGNANCY MONITORING
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By "pregnancy monitoring" we mean the activity of the gynaecologist in following the various stages of
gestation, diagnosing possible pregnancy problems. The world has changed a great deal in the last 50 years,
technology has made incredible progress, so much so that today's ultrasound scanners are certainly better
performing than those of several years ago.
The first thing to do is to diagnose pregnancy, i.e. whether a missed period is a pregnancy or a secondary
amenorrhoea (a blocked cycle). Nowadays it is very simple: it occurs with beta-HCG blood dosage, and using
much more powerful means than those available in the past. It is good, however, not to completely forget the
use of the hands, of semeiotics, in favour of instruments alone. ( Today we have, in fact, biochemical
investigations and a series of examinations and tools that make our work certainly easier; however, the ability to
diagnose, cure, and also increased the expectations of pz. )
It is important to evaluate:
- Signs of presumption general maternal phenomena: the increase in the volume of

the abdomen and the pigmentation of the dawn line, two changes that do not occur
the very first days of the non-cycle; pollakiuria, nausea, morning vomiting,
sialorrhea, changes in taste; the chloasma gravidarum (image on the side) may be
more pronounced and premature if the fetus is male and in the presence of dark
maternal complexion. Less cases of chloasma gravidarum are seen today: this
decrease is due to the fact that women are more educated than before about skin
protection during the summer period. All of these changes may make the doctor and
the pz suspect a pregnancy;
- Signs of probability the female genital apparatus changes, with an increase in the size of the uterus,
amenorrhea, hyperemia of the gingival mucosa, sense of breast swelling with hyperpigmentation of
the halo. At the beginning of pregnancy, in addition to amenorrhea and nausea, the woman reports that
her breasts have swollen: woe if the pregnant woman reports that she no longer feels her breasts
swollen, as it is almost always a sign of internal abortion.
- Signs of certainty can be found in the presence of the fetus by means of beta-hCG dosage, early
ultrasound, in which fetal heartbeat (BCF) and MAF (fetal active movements) can be detected.
The best evaluation would be the pre-conception one: it would be great to know the condition of the pz before
conception, and then follow it during pregnancy. This is because there are dangerous and life-threatening
diseases that should be treated or compensated for (such as diabetes) before seeking pregnancy. Possible
exposure to risk factors should be assessed, family history, an accurate obstetric, general EO and
gynaecological history should be made.
However, it is obvious that not all people get checked before a pregnancy for cultural or economic factors.
There is a type of visit, which is the private one, where the pz is checked periodically, starting already from puberty,
doing the various PAP tests, followed during the pregnancy, then for the menopause, and finally in the third age. In
the public, on the other hand, there are patients who are not constantly followed, who do not go to the gynaecologist
for 10-15 years, and are potentially those most in danger because absolutely nothing is known about them: it is
more difficult to make a diagnosis, and therefore it is easier to make some mistakes. It is also true that today the
ticket costs 46€, so if there was a greater health culture, probably prevention could be done even to the poorest
people, because for the lowest incomes the ticket is free. Often and willingly, therefore, the reason for these missed
visits is more for a cultural form, because often the pcs who had never gone to visit, when asked why, they answer:
"Because I was fine".
Preconceptive care
Before conception, appropriate treatment of sexually transmitted diseases, endocrinopathies, recurrent urinary
tract infections, diabetes, heart disease, anaemia, vitamin deficiencies, obesity, hypertension and any other
pathology that may complicate the course of pregnancy is necessary. Particular attention should be paid to
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patients in chronic therapies with potentially teratogenic drugs. So whoever gets checked first is definitely
more likely to have a peaceful pregnancy.
Risk factors for pregnancy:
- Maternal age (> 35): refers to pz as aged primipara. We know, in fact, that biological age and physical
appearance are completely different things;
- Paternal age (> 55): because you have, on average, already from over 45, a higher number of
spermatozoa with aneuploidy problems than young people.
- Presence of uterine malformations, or myomas, especially if they are intramural or submucosal;
- Bad social and economic conditions;
- Drug abuse, as well as tobacco or alcohol;
- Exposure to toxic substances or ionising radiation in the workplace . Of course, all substances that can
be teratogenic must be named during the history.
Anamnesis
The anamnesis must be collected carefully, especially if you have previous twinship, or if the current
pregnancy is twins; you must know if the pz is hypertensive, diabetic, if it has had congenital abnormalities
(chromosomopathies, neural tube defects, hemophilia, hemoglobinopathies, mental retardation). All these
things will have to be mentioned because, in such cases, the pregnancy will have to be followed with a pinch
of extra attention.
In case of familiarity with congenital abnormalities, the issue should be investigated to predict whether the
baby will be born healthy or not.
Of course, the obstetric history is also important: it is important to know whether it is the first child, possible
miscarriages, fetal endouterine deaths (MEF), preterm births, dystociae, growth defects or fetal macrosomies,
other neonatal pathologies (analyzing any clinical documentation of previous pregnancies: medical records,
instrumental and/or laboratory test reports, etc.). It is important because if something abnormal happened
during the first pregnancy, because it could happen again.
Preconception visit
The doctor will make the visit and ask for blood tests: blood group, Rh factor, possible indirect Coombs test,
complete blood count, blood glucose, kidney function, urine test, serological tests to assess whether you have
come into contact with rubella, syphilis, CMV, HVS 1 and 2, HIV, with all the various types of hepatitis and
toxoplasmosis. If the pz has no antibodies (it is receptive) for CMV, rubella and toxoplasma, IgG and IgM
antibodies should be detected at each monthly visit.
1st midwife visit
When a patient books this type of examination, it means that she knows she is pregnant (even through a simple
urine test), she will have some symptoms. If it is a pz never seen before, questions will be asked and different
examinations will be prescribed than for pregnant women who have already had routine examinations. Some
examinations, however, are to be redo, even if already done, because some become obsolete after 6 months and
some after 12 months.
The doctor will do a general EO, an evaluation of the genital apparatus and udders, ask for weight and height:
weight is important because it allows to assess how the pz is behaving during pregnancy, being ideal that the
pregnant woman does not take more than 11-13 kg. It will also measure the arterial blood pressure values, so
as to know, at time 0, what values the patient has, and eventually perform a PAP test, if more than a year has
passed since the last one (the execution of the same is quite optional, but it assumes importance in the pz that
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has never done it; even if in the public it is not always possible to do it, depending on the ticket that the woman
has paid).
Early obstetric ultrasound
It is important because, with the latter, you give an exact date to the embryo; this can be different from the date
obtained with the ruler, which is a calculation method based on a perfect woman, who has her period every 28
days, and ovules exactly on the 14th day. It can also be seen if there is a correspondence between uterus size
and the date of the declared amenorrhea: the woman can say a date, but if the size does not match, the
pregnancy must be re-dated. With the obstetric ultrasound scan you will be sure of gestational age, you will
have a correct dating of the beginning of amenorrhea and you will look for diseases affecting the uterus and its
appendages (thus being able to discover the presence of fibroids, ovarian cysts, or much more).
Historical digression: in the Official Gazette of '98 the Minister states that the pregnant woman can have
access to some laboratory and instrumental (minimal) tests in order to monitor the pregnancy, totally at the
expense of the NHS, while everything else is paid for: so if you want her to do some particular test, because
there could be a problem, she will have to pay for it, provided it is not exempt.
The patient should go to the gynaecologist within the 13th week, according to the Responsible Maternity
Decree: this is not what always happens, because some pcs do not realize
they are pregnant. This often happens in young and slightly fleshy girls, with
body fat masking the formation of pregnancy belly, and who think they only
have a delayed cycle. This is problematic because they may find themselves
in a band where abortion is no longer allowed.
Within the 13th week the State allows all the following examinations to be
carried out:
- Full blood count, blood type ABO and Rh, AST and ALT, blood
glucose, urine test.
- Serology: Rubella, Toxoplasmosis, Lue (TPHA and VDRL), HIV,
Indirect Coombs Test (only in Rh negative cases).
- Obstetric ultrasound scanning
Subsequent visits are planned with the gynaecologist: a pregnant woman should be visited once a month! And
then, once a week for the last 3-4 weeks to follow her safely to childbirth.
At the time of the first visit you have to evaluate the risk factors and possible embryopathies, possibly using
prenatal diagnosis techniques: probabilistic techniques tell you the probability that the child is healthy or sick;
there are techniques that go to study chromosomes, such as sexual ones, or problems related to 13, 18, or 21
(i.e. the chromosomes that most frequently give chromosomes).
Questions from the gynaecological visit

(it's also true that pz can't wait to tell you in detail how she is):
1) Is he asleep?
2) Tired?
3) Breathless?
4) Nausea, acidity, fasting, digests well, how many meals does he eat?
5) Do you have hemorrhoid disorders?
6) Constipation?
7) Loin-sacral pain?
8) Pollakiuria, burning during urination, tenesmo?
9) Cramping?
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Examining also the presence of oedemas and/or varicose veins.
The mother only has to fatten up to a certain amount:

Table VI comment in the slides: at 10 weeks the fetus weighs 5 grams, the placenta 20g,
the amniotic fluid 30g, the uterus 140g, the mammary glands 45, the blood 100g, for a
total of 340g. The actual increase in weight of the mother: 650 grams. With a "reserve of
energy", of mother's fat, 310 grams. Therefore, having a weight gain of about 600 grams,
a 10 week pregnant woman should not notice a weight gain, so much so that in many
sports women you absolutely do not see the belly
until 10 weeks.
The exams scheduled after the first 13 weeks are:
Week 14-18: urine test
Week 19-23: obstetric ultrasound and urine examination.
24th-27th week: if she is not diabetic or glucose intolerant before
pregnancy, a glucose mini-load is performed to see how her blood glucose
responds and how the patient's pancreas reacts;
28th-32nd week: complete blood count, ferritin, urine examination, and
obstetric ultrasound, this ultrasound is currently a question mark: this
would be, in fact, the third ultrasound to be performed by the NHS; (the
first is performed within the 13th week, the morphological ultrasound at
the 20th). This one from the third quarter some time ago had been
removed for budget reasons, although currently someone is being charged
to the NHS again.
33rd-37th week: complete blood count, urine test, and serology: the baby is about to be born and must not
come into contact with HIV, HBV. HCV, but the doctor also needs to know the patient's condition to protect
himself.
From the 41st week: Obstetric Ultrasound, serious cardiotocography, a machine that is used to check if the
woman has contractions and fetal well-being.
In case of significant bacteriuria we make urine culture with antibiogram; it is very easy that in a pregnant
woman there are many bacteria in the bladder and she has asymptomatic bacteriuria, because it changes the
anatomy of the genital organs and the relationships between rectum, vagina and urethra with increase of
bacteria in the urine. This is also demonstrated by the fact that it is easy to have a positive vaginal swab for
bacteria that should not be in the vagina.
IMPORTANT: The teacher also reminds that if the pz is receptive to CMV, rubella and toxoplasma, IgG and
IgM antibodies should be searched for at each monthly visit. (for example, if the patient has come into contact
with CMV and rubella for vaccinations or for having contracted the disease beforehand, while she is receptive
toxoplasmosis, this patient will have to do monthly Ab tests for toxoplasmosis).
In addition, every month we also check every reference parameter for a certain pz health problem (e.g. TSH in
case you have hypothyroid pz in therapy, until you have a TSH not perfectly balanced).
In the midwifery examinations carried out in the 3rd quarter of gestation, the so-called Leopold maneuvers
must be carried out.
Leopold's first manoeuvre with his hands is to look for the bottom of the uterus. It is also said
what is under the hands, for example a head, feet; obviously today you can know everything with
an ultrasound probe, but it is not a completely lost practice.
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Leopold's second manoeuvre is an attempt to obtain information about the fetal situation: "situation" means
the ratio between the longitudinal diameter of the uterus and the fetal cephalopodalic diameter. You also look
for an answer to the question, "Is his head down or his head up?"
Leopold's third manoeuvre We place our hands at the level of the pelvic excavation, where we can find the
head, and thus understand the degree of commitment, to know if labor is beginning. If the
commitment has not taken place, the doctor's hands manage to join together because the
child's head is missing; if the head, on the other hand, were in the pelvic excavation, the hands
would meet it, and they would not be able to approach each other.
Remember that sometimes the children are so big that when they
are pushed out, they create pubalgia, because as they pass the joint
heads of the pubic symphysis move away a bit and the pubalgia that is created can last from 6 to 12 months
after the birth.
It is then necessary to assess the development of the child, detecting prematurity and intrauterine growth
retardation of the child. With prematurity, it is observed whether or not the child corresponds to gestational
age; with intrauterine growth retardation it is seen whether the child, who had initially grown normally,
suddenly grows less: this change is a hallmark of a problem. These two parameters should be noted as they
have a major impact on perinatal mortality and morbidity rates.
OBSTETRIC AND GYNAECOLOGICAL ULTRASOUND
Obstetric ultrasound and gynaecology is now the basis of gynaecology.

The ultrasound technique has improved enormously over the years, so much so that you now have 4D
ultrasound scans; but it all started with Sonar which was used during the Second World War.
The first obstetric ultrasound was in 1958. Padua was one of the first locations, in 1960, to buy an ultrasound
machine in Italy.
Ex. Of ultrasound that allows us to see an embryo, with its head, nose, mouth,
belly, and ass between the 8 and 12 weeks of life, lying in the position defined
"fetal" and with the head about the same size as the belly.
The gestational age of such an embryo is measured by placing a pointer on the head
and calculating the distance from the thumb. (Standard CRL measurement).
The ultrasound can be of two types:

- Transabdominal
- Transvaginal
Transvaginal ultrasound can only be performed by a gynaecologist; but a gynaecologist also uses
transabdominal ultrasound to follow pregnancies. Until the 12th week of pregnancy, transvaginal ultrasound
can be used; from this 7th on, transabdominal ultrasound will be used.
What's the ultrasound for?
- To diagnose pregnancy
- Allows the localization of pregnancy
- To carry out Fetal Biometrics, that is to say to understand how the unborn future is growing up
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- To study the Fetal Annexes

- To control fetal well-being
- The study of malformations
The NHS guarantees three ultrasound scans, one in Q1, one in Q2 and one in Q3.
In private, whenever a patient has a visit, an ultrasound and fetal biometrics will be
performed.
In the first trimester it is essential to make a diagnosis of pregnancy; seeing the
gestational chamber, the calf sac and seeing the embryo, it will certainly be
possible to say that the patient has an intrauterine pregnancy. (In picture)
Also important is the possible diagnosis of an ectopic pregnancy, a situation that

could lead to the death of the patient if not diagnosed. There are, in fact, fetuses
that are not implanted in the uterus, but in other organs. Very often this happens at
the level of the TUBA, which has a very thin mucosa and this favours the embryo to implant itself at this level,
piercing the tubal wall until it finds an arterial vessel that allows it to survive. Women with this condition used
to die at night, suddenly, some without knowing they were pregnant.
This non-diagnosis was mainly due to the lack of ultrasound, b-HCG examination and serious
b-HCG. B-HCG in a uterine pregnancy doubles every two days, while it increases less characteristically in an
ectopic pregnancy. (This can be seen through b-HCG seriates)
Today, however, the possibilities for diagnosis and treatment are enormously greater.
Ectopic pregnancy can be:

Intrauterine
-Angular, near the tubular corners

-Cervical
Extrauterine
-Tubarica
-Ovarica
-Addominal
Ultrasound also makes it possible to study Evolutivity by analysing:
- The presence of a heartbeat; paying particular attention to its frequency. Tachycardia is, in fact, a
normal condition initially in the fetus, while bradycardia is an extreme risk situation, indicating a
probable abortion.
- The dimensions of the gestational chamber
- The size of the calf bag
- The presence of hematomas
THE TRIMESTERS
In the first trimester it is important to check the gestational chamber, the calf
sac.
At the beginning of the trimester the CRL, i.e. the cranio-inch distance, is
calculated, accepting as error +- 5 days; later in pregnancy the DBP, i.e. the
biparietal diameter or the length of the femur, can be measured.
All these measurements orient on the exact date of the last menstruation and
how long the embryo really has.
As morphology in the first trimester, the cephalic extremity, chest, abdomen and
limbs must be searched and seen clearly.
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It is also necessary, always in the first quarter, to search for the annexe fields:
- A possible corpus luteum (index that the patient ovulated)

- Possible swelling
- A heterotopic pregnancy
Without neglecting the study of a possible twinning, and in the case of several embryos, to understand if they
are mono or bicchorial, i.e. if they have a single placenta or two distinct placentas.
II TRIMESTRE
Between the 20th and 22nd week, the morphology is done, "the most beautiful ultrasound there is", where the
biometrics will be seen, checking the growth of the fetus, the fetal morphology, the fetal kinetics and the fetal
annexes. Dating is done by evaluating the following parameters:
- Bi wall diameter (BPD)

- Cephalic Circumference (CC)
- Femur length ( LF)
- The circumference of the belt/abdominal (CA)
It is necessary to control the rhythm of growth, which may be normal or there may be a growth retardation; in
case of growth retardation the etiology of the growth will be investigated, reassessing the patient's medical
history, comparing the previous ultrasound scans, and possibly helping with invasive investigations.
It is always important to make a :

- systematic evaluation
- with a caudal skull approach (each time you have to start from the study of the head and then go down.
NEVER start with your feet and then work your way up)
- the examination time must be adequate (times can be different depending on the skill achieved by the
doctor, but never exaggerate in excessive speed or excessive slowness)
The ultrasound also allows you to assess fetal kinetics, studying if there is normal
motor activity and good fetal tone.
Finally, we must evaluate the fetal attachments, remembering to look for two
arteries and a vein, and the amount of amniotic fluid.
III TRIMESTERS
This quarter we are talking about ultrasound of fetal well-being and growth. If the
baby has arrived at 30 weeks feeling well and the mother has not developed
complications, most likely the delivery will be serene. But even at this time you have to check it out:
-Biometrics
-Fetal Morphology
-Kinetics and fetal well-being
-Fetal attachments
As biometric parameters, in the third quarter, they are used:
- Bi wall diameter (DBP)

- Cephalic Circumference (CC)
- Abdominal Circumference(CA)
- Femur length
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Through this data, the gynaecologist can make a STIMA of the fetus' weight and the future unborn child,
imagining that the fetus will be born at 40 weeks.
Therefore, in general, the ultrasound is used for the management of pregnancy, gradually investigating how the
pregnancy proceeds; for fetal diagnostics and fetal well-being.
GYNAECOLOGICAL ULTRASOUND
It is an examination to assess the uterus, endometrial cavity tissue, ovaries.

This is the image of a healthy uterus, without fibroids, without myomas, with
trilaminar endometrium (like a mouth), always present at mid-cycle. Being halfway
through the cycle we can be sure of the presence of a dominant follicle, a follicle
that will soon burst either in the right or left ovary.
This is the image of a young patient's ovary. It's

multifollicular, full of eggs.
Studying the uterus is important:

- Measuring Diameters
- Investigate the presence of anomalies ( ex. Fibroids)
Endometrium:
- Thickness
- Phases of the cycle
- Anomalies
Picture: you can see the endometrium with a particular hyperecogenic zone, an
octopus.
Ovaries:
- The diameters
- Phases of the cycle
- Any Tumefactions
Image of a possible anecogenic cyst, therefore physiological or a growing follicle

(depending on the size you can understand if it is one or the other).
Picture of an endometrioma, an endometriosis cyst,

recognizable by its finely dotted appearance.
Finally, it is important to study all the neoformations with the eco-

doppler technique, which informs us if the capsule is fine or thick, if it is vascularized
or not, and if within the formation there is a so-called "token" and if it is vascularized
or not.
All this information will allow us to orient ourselves towards a benign mass or one with
signs of malignancy.
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The teacher then shows images of fetal reproductions, visible in the slides, currently available thanks to
advanced computer techniques. They are indicative images that make it possible to predict characteristics in
the unborn future, such as the presence of flapping ears and other general characteristics, without forgetting
that they are not photographs, but reproductions that can more or less approximate reality.
SEAT PREGNANCY ABNORMALITIES
A normal pregnancy lurks in utero. If the pregnancy test is positive and

the pregnancy does not nest in the uterus, we speak of a site
abnormality or ectopic pregnancy.
In this case the oocyte meets the spermatozoon in the tuba and then, as
it returns downwards, nests inside the tuba instead of continuing its
descent.
It may erroneously nest in the ovary, the tuba (most common place),
and at the uterus itself.
Pregnancy can be ectopic intrauterine or extrauterine. An example of
intrauterine ectopic pregnancy is the angular one. If you nest in the
wrong part of the uterus, this will still be a site abnormality, an ectopic
pregnancy.
The incidence is 0.25-2.5%, about one in 200 women. So it's not a rare condition.
Every year about 3000-3300 women give birth in Padua. About 15 people a day. (Long digression on the fact
that Padua is a third level gynaecological center, where there are not only Padua's birthing women, but also
difficult cases, non-natural births, those defined at risk that are sent here from other hospitals in the
surroundings. In 1960/70 about 8000 births per year took place here, but the medical-legal consequences did
not exist, breech births, twin births were done by vaginal way, there were not the right resources to
understand that the fetus was suffering and that it was better to induce the birth before the term, so obviously
the neonatal mortality was much higher than now. Maternal mortality was also, unfortunately, much higher.
Today is very rare. Maternal mortality is currently about 5 patients per year).
DURATION
ABORT
The termination of pregnancy before the 180th day is called ABORTION. After the
180th day, instead, we talk about FETAL DEATH.
It's called abortion because it happens before the fetus has the ability to survive. Today a
fetus of 23-24 weeks, with the right therapies, can survive. It will be a baby that will not
weigh more than 500g at birth (it will be in one hand).
Not all infants this small survive, moreover a high percentage of them will have small
learning disorders; they are children who seem normal, but in the schooling phase they
show learning difficulties, most likely due to small areas of anoxo-ischemia in some
areas of the brain.
PREGNANCY BEYOND TERM
We speak, instead, of pregnancy beyond the term, a pregnancy with delivery

after 42 weeks.
Going beyond this date is pathological, so much so that in Veneto at 41 weeks
and 5 days, in Padua 41 plus 3 days, doctors give birth to the pregnant woman.
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Ex. The gynaecologist will tell his or her patient to go to PS immediately, if within 41 weeks plus 5 days she
has not yet given birth, to induce a natural delivery or caesarean section.
The problems related to this delay are:
- Placental senescence (remember that the placenta at the end of pregnancy is like 90 years old )
- The increased risk of having MEFs, fetal endouterine deaths, often due to ischemic causes
- The excessive growth of the fetus
(The professor mentions that even diabetic women who give birth at the 39th week, so that the fetus does not grow
so much that it is difficult to give birth).
The incidence is 4-5%.
The correct dating of the pregnancy is done using ultrasound, following the patient from the beginning to the
end of the pregnancy. The case of patients who present themselves to give birth without ever having been
examined is different. In this case, having an ultrasound to see how big the child is is is much more complex.
For this reason, not only is the information given by the woman giving birth useful, but also the information
that the doctor collects with his own hands, seeing how tall the patient is, the type of pelvis she has, the
anatomical conjugate and the real conjugate (two important diameters), taking advantage of Leopold's
manoeuvres, to understand how big the baby is and its position. After gathering this information, with the help
of the ultrasound, the gynaecologist will have a more precise idea of the situation and will be able to choose
between a Caesarean or natural delivery.
The etiology of pregnancy beyond the term is mostly unknown, although it is thought that certain genetic
factors may contribute.
There is a need to monitor fetal well-being with:
- Cardiotocography
- Ultrasound scanning
Daily fetal movement counts at the end of pregnancy can also become important in some situations:
Ex. when a mother reports that the fetus was moving a lot during the rest of the pregnancy and recently
"doesn't move anymore". In this case you have to tell the mother to count the movements of the fetus daily,
movements that should never be less than 15/day.
Therapy
From week 40 monitoring to alternate days,
Childbirth at 41st week

- 41+2
- 41+3
- 41+5
- (Each clinic has its own number)
The professor reads the slide pointing out that to give birth to the patient can
be used both drugs to induce contractions and amniorexi, i.e. the rupture of
the chorionic amnio membranes, a laborious operation;
and that the elective caesarean section is preferred in some situations, such as
in case of fetal macrosomy, because the fetus could get stuck during its
descent to the upper-medium-lower excavation, with a strong risk of shoulder
dystocia (the gynaecologist's nightmare).
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Niccolò Ghiotto 10/10/2019, lesson4

Elisa Sartori Gynaecology, Prof. Ambrosini
Pathologies of the first trimester of pregnancy

ECTOPIC PREGNANCY
Blastocyst implantation in intrauterine pregnancy can occur in normal or abnormal sites, such as in the corner
or neck of the uterus, thus giving rise to an ectopic intrauterine ectopic pregnancy, respectively angular or
cervical. The implant in the cervix, as it is hyper-vascularized, can lead to terrible bleeding with consequent
hysterectomy. Ectopic pregnancy in the
extrauterine site with tubal implantation is
much more frequent, the more rare the ovarian
site and even more the abdomen.
The incidence of the phenomenon
is equal to 1 per 100 pregnancies
and 2-3:100 in case of IVF (in
vitro fertilization with embryo
transfer): the embryo normally
deposited in the uterus can still be
aspirated into the tubes and
implanted there . In case of
heterotopic pregnancy (situation
where a normal pregnancy inside
the uterus and an abnormal
pregnancy coexist) the incidence is 1:10000 and 1:100 in IVF.
Mortality is 1:2000 ectopic pregnancies leading to 3-4 deaths per year.
The risk factors are:

- Pre-existing tubal surgery, due to possible impairment of normal anatomical conformation(OR 21)
- Pregressa GEU - extrauterine pregnancy(OR 8.3)
- Pelvic inflammatory processes, inflammatory diseases that can ascend involving also the tubes (OR
2.5)
- IUD, an intrauterine contraceptive contraceptive device that sets up endometritis acting as a foreign
body (OR 5).
- Smoking
- IVF
- Tubal sterilization, with nesting of the embryo in the residual tubal stump for non-optimal surgery
(OR 9.3)
- Endometriosis and Endometriosis, being inflammatory processes can compromise motility and
geometry of the apparatus.
Genetic and endocrine factors can contribute to the etiology. The spermatozoon normally meets the oocyte in
the distal part of the tuba and in 4-5 days the product of conception migrates into the uterus as it develops. If
this is accelerated the fertilized oocyte implants first, usually in the proximal portion of the tuba. Chromosomal
anomalies can also lead to an altered timing of maturation and consequently to early implantation.
A slow descent of the fertilized oocyte also affects the implant site. This may be due to anatomical tubal
alterations, such as ciliated mucosa, often associated with inflammatory processes.
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Generally, if the ectopic pregnancy took place in the proximal area of the tuba, endocrine or genetic problems
can be assumed; if it takes place in the distal area, the cause must be sought in inflammatory processes that
alter the motility of the ciliated epithelium or an adhesion that limits normal tubal peristalsis.
An accelerated transit of the fertilized oocyte can instead lead to a cervical pregnancy, with terrible bleeding
complications. This can involve a hysterectomy while a tubal pregnancy can be resolved by a simple total
salpingotomy or linear salpingotomy with local embryo removal.
The usual outcome of an extrauterine pregnancy is an early or late miscarriage.

If the site is intrauterine the therapy consists of a scraping or the use of an antitumor (methotrexate) which, by
indiscriminately blocking cell replication, also has effects on normal gametogenesis, which is why it is
recommended to postpone a new pregnancy until the following year. You tend to avoid use of this medication
precisely because of the irreversible waste of time of procrastinating.
If the pregnancy is angular the surgical removal is generally simple and with little risk.
The symptomatology varies according to the evolutionary evolution, going from silent to an abdominal pain up
to an acute abdomen, due to a tubal rupture or massive hemoperitoneum, up to a shock.
Early symptomatology can be poor and is directly proportional to embryo growth.
Diagnosis
Experience, instruments, haematochemical tests and hands are essential. Normally you should feel a
consensual increase in the uterus of large and soft consistency. Pathologically, an evaluation of the tubes can
detect small nodes, more easily at a late stage.
Pregnancy testing and history will be as positive as the consensual increase in hCG, the quantification of which
is of paramount importance.
When in a normal pregnancy the value should continue to increase, doubling from time to time in the
extrauterine pregnancy there are fluctuating results, with increases and decreases. In abortion, the value
achieved decreases to zero.
In differential diagnosis, you have to ask:

- Intrauterine pregnancy
- rupture of corpus luteum cysts, which can result in a major effusion into the Douglas
- Ovarian cyst torsion, distinguishable for precise pain localization
- Acute pelvic inflammatory disease, often due to chlamydia or mycoplasma
- Ovarian abscess
- Endometriosis cysts
- Acute appendicitis: both surgical and gynaecological evaluation is fundamental in the suspicion
- Acute pyelonephritis
The therapy varies depending on the location of the implant.
In tubal pregnancy generally with the wait the problem is self-resolved and hCG is negative, the medical
therapy involves the use of methotrexate, surgically the way is laparoscopic, saving the open only in urgent
cases. Normally a linear, sometimes total salpingotomy is performed.
For completeness I report the other therapies by location

 Ovarian pregnancy:
 Early diagnosis: first methotrexate then surgery.
 Late diagnosis: surgery
 Laparoscopic resection Salpingostomy
 Ovariectomy
 Cornual pregnancy:
 Early diagnosis: first methotrexate then surgery.
 Late diagnosis: surgery
 Laparoscopic cornual resection
 Salpingostomy
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 Hysterectomy
 Abdominal pregnancy:
 Surgery
 Laparoscopic placental resection(60%)
 Intestinal resection
 Marsupialization gravidarum sac around the laparotomy wound
 Cervical pregnancy:
 Surgery
 uterine aa embolization
 Suction
 Cauta Cervical canal and uterine cavity revision
 Hysterectomy
Acute presentation must be followed by a hospitalisation with all the necessary precautions. Remember for the
umpteenth time that in the E.R. a venous access should never be denied to anyone.
ABORT
The incidence increases with age, from 13/100 in the third decade to 30/100 over 40.
Given the smaller number of children, the problem has taken on much more importance than in the past, when
it was considered normal.
Curiosity: the scraping, you see, was practiced by healing the uterus with knitting needles.
The professor will later point out how neonatology has reached a point where fetuses of the lowest weight of
500g can survive after the 23rd week. It has been observed, however, that these are highly likely to develop
neuropsychiatric problems that are normally delayed during the second, third grade with the demand for higher
and higher cognitive performance.
It's called an abortion:
- A pregnancy that has its term before reaching vitality
- according to WHO: The expulsion of a fetus weighing less than 500g
- for clinical practice: pregnancy term before the 23rd week of gestation which is variable from
centre to centre (temporal cut off for the fetus' independent life)
It can be classified in :
 Pre-embryonic if it happens before the 5th week
 Embryonic: between 5-9 weeks of pregnancy
 Fetal between 10-22 weeks
The sooner the abortion happens, the less psychological impact it has.
Abortion can be occasional if the episode is isolated and preceded in history by a normal pregnancy. The
Incidence is 8-25% and increases enormously over the age of 40.
80% of abortions occur in the first quarter, after the thirteenth week is unlikely.
Abortion is recurrent when two or three consecutive episodes follow. It can be primary or secondary depending
on whether it is preceded by a normal pregnancy or not. The degree of concern is proportional to the degree of
poliabortivity. The higher the incidence, the lower the number of epidoses, from 3% with two abortions to 1%
with three.
When occasional abortion may be normal, the claimant deserves further investigation.
Abortion can also be defined:
- Internal, if there is a failure to expel the abortive material and the embryo mummifies acting as a
foreign body predisposing infections. It can be removed with scraping, an easy gynaecological
technique that consists of endometrial curettage after enlarging the cervix with Haller's retractors. The
common mistake of the beginner is to pierce the uterus with the curetta when there is a physiological
curvature between the neck and the body to which attention must be paid.
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- In act, if the cervix is dilated with expulsion of deciduous-ovular material

- Incomplete if after expulsion of the abortive material there is abundant residue in cavities
- Complete, with no material in the cavity after expulsion of the abortive material
The diagnosis is clinical, instrumental and laboratory-based.

Patient usually shows up in the E.R. complaining:
1. Genital blood loss
2. Cramping pains in the lower abdominal quadrants
3. Cervical dilatation
4. Spillage of deciduous ovular material
5. Breast turgidity reduction
6. Possible hyperemesis resolution.
(He will hardly report the last two points at first)
The main test is the ultrasound that can show:

 An anembryonic ovule chamber > 18 mm
 An ovular chamber < 18 mm unchanged for 7 days
 An absence of cardiac activity in embryo > 5 mm
 An absence of growth or heartbeat after control at 7 days with embryo < 5 mm or a gestational
chamber < 20 mm
Laboristically, hCG decreases to zero.
The etiology is varied, it may be due to:

 Fetal chromosomal abnormalities (>70%, mainly in the first trimester) such as autosomal trisomies:
most do not allow embryo development. Chromosomal examination can only be required in case of
polyabortivity.
 Fetal morphological abnormalities
 Anatomical abnormalities, such as fibroids, sinecules (adhesions), cervical incontinence or uterine
variants (bicorne, unicorne, dideldo)
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 Maternal endocrine abnormalities (DM, dysthyroidism, hyperPRL)

 Maternal immune abnormalities such as antiphospholipid antibody syndrome
Antiphospholipid antibodies syndrome
Presence of venous thrombosis
Presence of 3 or more abortions
Presence of pre-term parts
Presence of anti-cardiolipin antibodies
Presence of lupus anticoagulant (LAC)
Incidence 10-20% of women with poliaboractivity
 Hereditary thrombophilic defects due to microthrombi formation often associated with late
complications such as placental detachment, preeclampsia. They can be controlled with anticoagulants
during pregnancy.
o Increased thrombotic risk
 Formation of microtrombi at the uterus-placental level
 Early complications
o Abortion I and II quarter
o 23% of patients with poliabortivity
 Late complications
o IUGR, Pre-eclampsia, Placental detachment, MEF
 Infections , typically CMV, syphilis but also parasites and fungi

 Chemical agents
 Idiopathic
The therapy can be surgical by scraping. If the endometrial thickness is less than 15mm you opt for a waiting
line. Medical therapy consists of the administration of prostaglandins typically after the 14th week. The
psychological aspect is important.
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HYPEREMESIS GRAVIDARUM
This pathology must be distinguished from normal vomiting during pregnancy.

Vomiting during pregnancy is considered normal in the first few weeks, is mainly morning and is associated
with typical pregnant sialorrhea. It usually has a benign development and disappears after the first trimester.
No therapy is really effective, ginger is an excellent natural antiemetic.
Hyperemesis gravidarum, on the other hand, leads to very severe nausea and vomiting, resulting in loss of
fluids and dehydration, loss of weight due to lack of food and ketoacidosis with dysmetabolism.
The incidence is 1/750 pregnancies.
The differential diagnosis should be placed with:
 Hepatopathies
 Kidney infections
 Pancreatitis
 Intestinal occlusions
 Intracranial injuries
The therapy aims to restore the hydroelectric balance with continuous infusion, such as the administration of
antiemetics, psychological support and progressive reintroduction of food.
GESTATIONAL TROPHOBLASTIC DISEASE
Hydatiform grinding wheel

Gestational trophoblastic disease includes the hydatiform mola (1/1500-
1/2000 pregnancies) which may be complete or partial with possible
evolution towards choriocarcinoma. It is characteristic of age over 35
and is associated with vitamin A deficiency.
Even at the beginning of pregnancy the patient complains of strong

nausea and hyperemesis, very high levels of hCG are found in the blood.
The diagnosis, easily suspect from the clinical presentation, is then
confirmed by ultrasonography with typical visible alterations after the 7-
8 gestational week.
The complete hydatiform Mola lacks recognizable fetal tissue and there is
a swelling and hyperplasia of the trophoblast. It is due to a chromosomal
imbalance for which an empty egg is fertilized by a paternal
spermatozoon which then duplicates forming an arrangement typically 46
XX.
In the partial hydatiform grinding wheel there is the presence of

recognizable fetal tissues, swollen chorionic villi with a considerable
irregularity of the edge and hyperplasia of the trophoblast.
Etiologically it is due to the fertilization of a normal egg with a
spermatozoon that then duplicates its genetic heritage.
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Hardly the product of conception comes to an end.
The complete hydatiform grinding wheel clinic includes:

 97% abundant vaginal blood loss
 50% excessive increase in uterine volume
 Excessive uterine growth rate
 27% preeclampsia
 Hyperemesis gravidarum
 7% hyperthyroidism
 2% trophoblastic embolism
 50% techno-lutein cysts
Partial hydatiform grinding wheel, on the other hand, leads to symptoms analogous to a complete or deemed
abortion. Diagnosis on histological examination involves 72% bleeding.
A suspicion is raised if a dead embryo, a hyperdeveloped trophoblast or a trophoblast cyst is found on the
ultrasound.
The therapy typically consists of:
 Hysterosuction + Curettage
 Hysterectomy
 Preventive chemotherapy with Methotrexate for developmental fear in choriocarcinoma
Choriocarcinoma
It can evolve in 10-20% after emptying by grinding wheel, presents with recurrent bleeding, with uterus with
asymmetrical enlargement and persistent high hCG levels.
Trophoblastic cancer is divided into:

- Stage I: elevated hCG, uterine confined tumour
- Stage II: Vaginal or pelvic metastases
- Stadium III: Pulmonary metastases
 Stage IV: Cerebral, hepatic metastases
The therapy consists of, depending on the case in:

- Chemotherapy (methotrexate, actinomycin D, etoposide)
- Hysterectomy + chemotherapy
- Hysterectomy + chemotherapy + radiotherapy
The follow up is performed with the dosage of hCG.
Survival in the case of a low-risk tumour is 90-100%, if at high risk it reaches 60-80%.
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Prenatal diagnosis
The prenatal diagnosis is used to see if the baby is healthy, today most couples make it except those who reject
it for ethical reasons. Maybe:
 Invasive:
o Villocentesis
o Amniocentesis
o funicolocentesis
 Non-invasive (involves the removal of fetal cells and allows the chromosomes to be analysed):
o Examinations on blood or urine from the mother
o ultrasound scanning
. Blood and maternal urine tests are all over it:
 Common blood tests
 Emogruppo Rh factor
 Glycemic curve
 Antibody research
 Metabolic studies
 Cytogenetic studies
SOFTMARKERS
Other specific markers, called softmarkers, may be indicative of fetal alterations, in particular:
- fetus protein
o High neural tube values
o Low valuesassociations with trisomies
- hCG
o High valuesassociations with trisomies
o High values associations with preeclampsia and IUGR
- Estriolus
- Pregnancy-Associated Plasma Protein A
All these are probabilistic indications, they do not allow for automatic diagnosis, but put together they can give
a reliable diagnosis based on a probabilistic system. We have gone from the analysis of the 1980s when,
without great reliability on the basis of a single marker, we were alarmed or not, to today, when soft markers
and ultrasound allow us to do a test that is probabilistic but highly reliable.
CORRELATION BETWEEN MATERNAL AGE AND DOWN SYNDROME
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The following table analyses the probability that the fetus carries a trisomy 21 (the anomaly responsible for
Down syndrome) depending on the age of the mother. Not all trisomies are considered because many do not
even allow the viability of the fetus. Trisomy 21 is famous because the defect allows the child to survive and
therefore its birth can be a "problem" to deal with (particularly economically). There were and still are
chromosomal anomalies that allow the survival of the child despite causing important morphological
anomalies (in the past these children were called monsters and were locked up in institutions). Today, it is
often the families who take full responsibility for these situations. The professor cites the example of autistic
children who can benefit from specialized learning institutions but at a monthly cost of 1500€, when the state
grants only 500€ as a monthly subsidy.
This table shows that at the age of 20 the probability of giving birth to a child with Down's syndrome is 1/1527
while a 45-year-old has a 1 in 23 chance that the child will have trisomy 21 (which is by no means little). This
is in support of the fact that having children as old people is not only more difficult and there is an increased
likelihood of abortion, but also increases the likelihood of the fetus being sick.
This concept is particularly delicate because it concerns any kind of doctor (and not only the gynaecologist)
because as such he has to give information to women or couples: children have to be made when they are
young and if you can't do it within a certain age you have to go to a specialist. The first causes are coming to
gynaecologists who did not warn patients that they might be at risk of not having children because of their
biological age (which must be distinguished from their age and can be assessed through particular
examinations that assess the ovarian reserve - i.e. ovarian function and follicular heritage according to its age -
because even if you are young aesthetically the age of menopause is not the same for everyone).
Another concept that the professor intends to point out concerns general practitioners, who sometimes tell
patients who have turned to medically assisted procreation that they disagree and judge the hormonal intake it
involves to be excessive. The general practitioner does not have to agree but has to be cultured and prescribe
the appropriate medication. His ethical thinking must not in any way affect these choices. They must also refer
patients to a specialist if they have not yet managed to have children at 40.
NON-INVASIVE TESTS
THE TRIPLE TEST
He went for the major until about ten years ago and understood:
1) Alpha fetoprotein;
2) Beta hCG;
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3) Estriolus.
Depending on these three values, the patient's risk level was defined as low to medium to high. Sensitivity and
specificity of this test are very low.
Diagnostic capacity = 57%
COMBINED TEST DUO

It's still a great test today and it's also called ultra-screen. We look at free βHCG, A protein and estriol, then
ultrasound to check nasal bone (which is absent in children with Down syndrome) and nuchal translucency
(which has increased in the same children). The sensitivity is so high that it has been the benchmark test for a
long time, also because it is non-invasive. In this way, the patient can only investigate with invasive tests in
case of positivity. (it was therefore suitable for young, not anxious women).
Diagnostic capacity = 90%
DNA AMPLIFICATION
Now a test has arrived in Italy that is not covered by the NHS but allows to isolate the cells of the fetus from
the maternal blood and perform a chromosomal mapping. It's very popular, but also very expensive, although
who can afford it.
For 8, 13, 21 and sex chromosomes it is about 650 €, but it can reach 4000 € by analyzing all the chromosomes
and also particular pathologies or microdeletions. The result is usually after 5 days.
The indication is certain with a single blood sample. It is the future even if it is not certain that it will be
provided by the NHS.
Diagnostic capability =99.9%.
90% of patients do the DNA test (referring to an economically normal target).
INVASIVE TESTS
VILLOCENTESIS
The ultrasound probe can be used to make an invasive prenatal diagnosis, which is excellent because it gives
certainty but involves entering the uterus with a needle. It can be early (villocentesis): you enter with a fairly
large needle that goes to perforate skin, fat, fascia and finally the uterus, you go to take the pieces of placenta
(depends on whether it is in front or behind) that you take and analyze. 21 days later you have the result. The
risk is minimal if the operator is experienced. You go get the fetal part of the placenta, not the maternal part. It
is an eco-guided procedure; if the placenta is anterior it is easier but if it is posterior it is enough to move the
needle and change the angle, also to avoid the child. The risk of abortion is around 0.5-1%.
AMNIOCENTESIS
Amniocentesis is performed between 16 and 18 weeks and consists of aspiration of amniotic fluid. It is simpler
as a procedure than villocentesis. The risk of abortion is 1/1000.
It can also be carried out late but does not make much sense except for some particular pathology. There is also
the very early one, which is already taking place in the 14th week.
The needle does not have to be inserted very deep to aspirate. All
it takes is 12-20 ml of amniotic fluid and during this procedure it
is feared that it will not take enough cells because they are diluted
between the urine and the desquamation of the child. The risks of
this procedure are:
1) Infections;
2) uterine hypercontractility because you go to stimulate the
uterus by piercing it;
3) the membranes rupture if they accidentally perforate.
The first amniocentesis in Italy (1965-1966) performed with a
fairly rudimentary ultrasound machine hesitated in a perforation
of the fetus. Today ultrasound scanners are very high performance, but there is still the risk of stinging the
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child or the child touching it as it moves. In any case, it is known that every surgical procedure involves a risk,
although the operator is very experienced.
This examination allows to carry out the karyotype and is dispensed by the NHS and therefore if the mother is
anxious, if there is a previous child with trisomy, if you are carrying chromosomal translocations or
mosaicisms you choose to carry it out.
Echo-guided procedures today are much simpler thanks to the translucency of the needles and the higher
resolution of the ultrasound scanners. The pointer was once used to orient the needle because it was not very
visible through the ultrasound probe.
FUNICOLOCENTESIS
The funiculocentesis is not done; it consists of a direct collection of fetal blood in the umbilical cord where
there are two arteries and a vein: you have to enter the vein and aspirate. It's not easy at all and it's very
dangerous. It is performed after the 20th week and includes a 3% risk of fetal death.
PHAETOSPIA
you enter with a camera to see the fetus and its external malformations. There is a good chance of assessing
whether the fetus is normal or not but it can result in high fetal loss (10% risk of killing the fetus for a control).
However, the utility is there for TTTS (twin to twin transfusion syndrome). In fact, in twins, particularly
monochorial twins, there can be a twin who eats a lot (polycytheemic) and one who eats less (anemic). This is
due to the fact that collateral vessels have formed that also seize each other's blood. A coagulator is used to
close the anastomoses that seized the flow to the anaemic twin, in the hope that a normal situation will return
to normal and that both fetuses will be equally transfused. The continuation of this situation would inevitably
result in the loss of at least one of the twins, so it is worthwhile doing so despite the high risk of fetal loss
(which is not justified in the case of a simple check-up).
Zanella Luca 16-04-2019

Pasin Cristiano Fisiatria -
lesson 2
Tuppo Vittorio Prof. A.
Frizziero
Balconetti Erika
TENDON AND TENDINOPATHY

Prof. Frizziero declares that he will attend the lecture and will integrate the explanation of Dr. Gamberini, a
first year specialist in physiatry, who follows the content of the slides (he reads them!).
The professor's interventions are reported in italics.
A brief introduction by Prof. Frizziero who announces that in the afternoon he will give a lecture with focus on
ultrasound. Remember that when a radiological image is requested as a resonance, it is always necessary to
specify the diagnostic suspect to be settled.
Tendon pathologies will be treated today. These are very frequent pathologies and very difficult to treat
because they affect a tissue that hardly responds to therapy. Padua is a centre of choice for tendonopathies.
Tendon Anatomy and Physiology

Tendons and ligaments can be considered as machines with several moving elements organized in such a way
that the force is transferred to and from the skeleton. They're organized in fibrils, fibers and bundles, units
getting bigger and bigger. The primary fascicles are covered with a band called endotheneonium; the primary
beams are organized into secondary and tertiary beams. The tertiary beams form the tendon which has an outer
coating called epitenonium.
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So the tendon is a multifibrillary structure with wrapped bundles organization, through a screw arrangement
between them (like the top of a ship). This configuration gives greater tensile capacity to the tendons, which
are better able to withstand loads, and the elastic component is also better exploited.
They connect the muscles to the bone and form the muscle-tendon unit whose main function is to transmit
tension loads generated by the muscles in order to move and stabilize the joints. This unit is a frequent site of
overload and motion related diseases.
Tendon characteristics:
• bright white color;
• fibroelastic structure;
• variability of the shape according to the area in which they are placed.
From a histological point of view, 90-95% of the cellular component is composed of tenoblasts and tenocytes
and 5% of other cells, such as chondrocytes near the entheses, synovial cells near the sheaths and endothelial
and muscular cells that make up the arterioles.
Tenocytes and tenoblasts are immersed in connective tissue, 65-80% collagen type I fibres and 2-3% elastin
fibres.
In summary, the tendon fibers are grouped into primary, secondary and tertiary bundles, each wrapped by
reticular connective tissue called endothenonium. A group of tertiary beams form the tendon which is
surrounded by epitenonium. The majority of the tendons are wrapped in connective tissue called peritenonium.
Some tendons of hands and feet are wrapped by the synovial sheath formed by two small sheets, one visceral
and one parietal, within which synovial fluid is present.
Endotenonium is the lining of the files present in the tendon and works like the omentum of the intestine. On
the outside of the files is epitenonium, coated externally with peritenonium. Epitenonium and peritenonium
perform the same function as the parietal and visceral pleural leaflets in the lung, which flow between them.
The peritenonium is a small leaflet found in the large central tendons, whilst in the peripheral tendons,
smaller, of hands and feet, there is no peritenonium, but a synovial sheath. This happens because even though
peritenonium does not produce much synovial fluid, a large central tendon flows well and only needs
protection, while peripheral tendons need more flowability. In fact, you can flex your fingers in maximum
extension of the wrist, making complex movements under the retinaculum. The sheaths therefore produce a
viscous liquid that allows the tendons to slide without friction and the movement is fluid.
There are 3 different cladding structures:

1. epitenonium: a 10 nm coating consisting of connective tissue with collagen fibres oriented obliquely,
longitudinally and transversely. There are also vascular, lymphatic and nervous structures;
2. peritenonium: covers tendons without synovial sheath and consists of collagen type I and III. It is an
elastic membrane that allows the sliding of the tendon;
3. synovial sheath: present in small joints. It is a sleeve consisting of 2 sheets, one parietal and one
visceral. Inside there is synovial fluid, whose functions are to promote flow and nourish the tendon.
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The tendons anchor firmly to the bone through the osteo-tendon junction, reinforced by large bundles of
collagen fibers also called Sharpey fibers that deepen into the bone. There are 4 zones in the osteo-tendon
junction:
1. tendon;
2. fibrocartilage;
3. calcified fibrocartilage;
4. bone.
Depending on the area involved, the prognosis changes.
Tendons have a reduced vascular supply compared to muscles (metabolically more active). Tendons receive
blood through three main systems: two intrinsic systems, located at the osteotendinous and myotendinous
junctions, and an extrinsic system, through the peritenonium or synovial sheath, the external linings that come
into contact and bring nourishment to the tendon.
The vessels originating from the muscle generally extend from the myotendinous junction to the proximal third
of the tendon, while those originating from the osteotendinous junction are limited to the insertion area of the
tendon and communicate with the periosteal vessels. The vascularization of tendons is compromised in
junctional areas and at sites of torsion, friction or compression and tends to decrease with age. Areas with little
or no blood supply represent the most common sites of degeneration and/or tendon rupture.
Studies in which Doppler ultrasonography has been used suggest that tendon vascularization in some
individuals may vary from day to day, depending on the amount of exercise performed and the subject's
metabolic activity (at rest or under stress). Blood flow in peritendinous tissues increases in response to intense
physical activity.
Biomechanical characteristics of the tendon:

• tensile strength: organization of collagen fibers;
• adequate flexibility: properties of elastin fibres;
• inextensibility: necessary to transmit forces to both bone and muscle;
• reduced resistance to shear and compression forces;
• Shock absorption: limits muscle injuries.
Most human movements are characterized by an eccentric muscle contraction phase, immediately followed by
a concentric phase. The muscle-tendon unit accumulates elastic energy during the eccentric phase and
mechanical energy during the concentric phase. These two types of energy accumulated in the tendon are able
to lead to overload pathologies and are to be dosed in the therapeutic program.
In the shortening and stretching of the muscle, actin and myosin fibers flow over each other. In a flexion of the
elbow the biceps shorten, the actin and myosin come closer and the sarcomere shortens; in this way
mechanical energy is accumulated. Following the elongation of the biceps the mechanical energy is released in
the eccentric phase in which the sarcomere stretches. In the eccentric phase the tendon lengthens and elastic
energy accumulates. It has been demonstrated that in eccentric exercise, i.e. stretching the muscle under stress,
this stretching is transmitted to the tendon that accumulates elastic energy. This energy allows to give a
mechanical and biological stimulus to the tendon itself, with greater activation of the cellular component and
deposition of elastic fibers, so the tendon tends to remain more elastic. Eccentric exercise can prove
therapeutic if administered in the right amounts.
The tendon is very strong because it has a high tensile force of 50-100 N/mm2, is able to stretch up to about
4% of its length at rest and accumulates 70% of the total elastic energy alone.
Tendon Pathologies
Terminology:
• Tendinopathy: clinical condition characterized by pain, swelling, functional limitation in and around
the tendon resulting from functional overload
• Tendinosis: degenerative pathological condition with absence of changes of inflammatory origin with
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disorientation of collagen, disorganization and separation of fibers due to a mucoid substance.

• Peritenonitis: inflammatory condition involving peritenonitis associated with neoangiogenesis
In outpatient clinics tendon pathologies are usually related to overload situations.

About 50% of all sports injuries are secondary to overload. The majority of injuries found in runners are
related to overload and about half of these involve leg (20%), ankle (15%), foot (15%).
More than 30% of sports injuries are related to tendinopathy, with a prevalence of patellar tendinopathy in 45%
of volleyball players and 32% of basketball players, achilles tendinopathy in 29% of runners, lateral
epicondylitis in 40% of tennis players. The tennis player's elbow is linked both to overload situations and to
materials that do not absorb the forces well.
However, tendinopathies are also frequent in the general population who do not practice sport, in sedentary
people, which is a risk factor for tendinopathies.
Tendinopathies are more frequent in men: the prevalence of tendon pathology in men would be related to a
protective action of estrogen on tendon structures in women.
The reduction in circulating levels of estrogen (as in menopause) leads to a reduction in the protective action of
these hormones. In the tendon there is reduced tensile strength, reduced collagen turnover and reduced
expression of aggrecans and other proteoglycans (biglicans, decotin, versicans), which are important to
maintain the elasticity of the tendon.
Risk factors may be:

• Intrinsic
 systemic: age (reduces blood supply), obesity, diabetes, hypertension, dyslipidemia (lipid
accumulation in the tendon) and genetic factors;
 non-systemic: biomechanical abnormalities (skeletal alterations such as knee launch/valgus),
reduced muscle elasticity (contractures), reduced muscle strength, joint laxity;
• Extrinsic: overload, incorrect training, incorrect equipment (if you run with the Converse the heel is
not properly cushioned by the sole) and drugs such as fluoroquinolones, steroids, hormonal therapies,
oral contraceptives, NSAIDs, retinoids.
It is predictable and well documented in literature that tendonopathies appear more often in athletes who
frequently change the type, intensity and duration of training.
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In the past, very old training methods were used. For example,
the athletic trainer at Inter in Cúper had the players do running
shots in the sand with teammates on their shoulders, keeping
the same load and training intensity for two athletes with very
different masses. Clearly the overload was different.
An imbalance between training loads and rest periods can lead

to fissures and injuries in the tissue.
Ex in photo: patellar tendon injury
The intensity and frequency of tendon tissue elongation affect
the biochemical responses of tenocytes and the mechanical
properties of collagen fibers.
The effects of controlled and repeated stimulation in terms of intensity and frequency applied to tendon
plasticity are not yet well known. This aspect is being studied a great deal in the literature, especially with
regard to rehabilitation and therapeutic protocols for the dosage of the intensity of the stimulus to be given to
the tendon.
The exercise stimulates an increase in collagen synthesis and degradation, but the synthesis prevails and lasts
longer than degradation, with an overall effect that induces an enlargement and strengthening of the fibres.
Therefore, exercise improves the tension-elastic properties and makes the tendon more resistant to mechanical
stress. This in physiological, normal conditions, where there is a balance between concentric and eccentric
strength.
The mechanical capabilities of the tendon depend on the precise alignment of the collagen fibres and the
expression of proteoglycans. These give the typical viscoelastic properties to the tendon, protecting it during
the execution of moderate to intensive efforts.
Overload
When the tendon is subjected to overload and repeated strain, the collagen fibers begin to slide over each other,
breaking the cross-links and causing denaturation of the tendon tissue. This creates alterations in the
extracellular matrix and vascular elements of the tendon.
Collagen fibres are very important, as they are structural; alterations of these lead to the onset of
tendonopathies over time.
Modifications of collagen fibres:

• collagen fibre degeneration with disorientation and thinning
• increased degradation of collagen compared to synthesis
• increase in interfibrillary glycosaminoglycans
• reduction in collagen type I content (more elastic)
• increased collagen type III content (less elastic)
Modifications of cells and extracellular matrix:

• increased cellularity (with non-functional cells)
• increased production of cytokines (e.g. IL-1β)
• increased production of pro-inflammatory agents (Cox-2, metalloprotease, ADAMTS), with
destruction and reshaping of the extracellular matrix
• neovascularization, prerogative to inflammation
Overloading also leads to hypoxia and ischemia of the tissue with production of free radicals, excessive heat
production that is not good for the tendon, apoptosis and NO deficiency, whose function normally involves
vasodilation and consequent increase in blood flow, inhibition of platelet aggregation, inhibition (at high
concentrations) of angiogenesis, inhibition of leukocyte adhesion to the endothelium, inhibition of proliferation
of smooth muscle cells of the vascular wall, antibacterial and immunomodulatory activity.
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Nitroxides are highly deleterious in the joint, especially if damaged and arthrosic. In tendons, on the other
hand, nitroxides can play a therapeutic role, so much so that nitroglycerin patches are often used in the
tendon.
Q: What is the role of ozone infiltration?

A: there is no scientific evidence of efficacy outside the context of the paravertebral musculature of the rachis.
The principle is that of deep tissue oxygenation, with effects also sclerosing and on neoangiogenesis, but it is
all still to be studied.
Tendinopathy
Tendinopathy is therefore a clinical condition characterized at the tendon and peritendinous level by pain,
swelling and functional limitation. It is a pathological condition characterized by the presence of degenerative
lesions and not inflammation.
For many years there has been talk of tendinitis, but this in itself does not exist; the inflammatory process
affecting the tendon itself cannot be detected and even in biopsy samples taken in widely degenerated tendons
it is not possible to detect an increase in inflammatory cytokines. On the other hand, the inflammatory process
mostly affects the membranes covering the tendon, with phenomena of neoangiogenesis and the formation of
new peripheral nerve endings, which are responsible for painful symptoms.
The term tendonitis should therefore be reserved for histopathological diagnoses.
This definition of tendinopathy was formulated in 1998 by three sacred monsters of degeneration
tendinopathy: Prof. Maffulli (Director of Sports Pathology in London, Medical Director of the London
Olympics, Ordinary of Orthopaedics in Salerno), Khan KM (Editor in Chief of the British Journal of Sports
Medicine) and Puddu G. (Ordinary of Orthopaedics in Rome "La Sapienza").
Also Arnoczky, one of the most important authors and researchers of mechanobiological phenomena of
peripheral tissues, has seen that for a long time it is possible to have degenerative lesions without realizing it
and to develop a painful tendinopathy only late.
Subclinical damage can occur long before the appearance of painful symptoms and this is typical of all
degenerative pathology of the musculoskeletal system.
The diagnosis is clinical, supported and confirmed by laboratory tests and imaging investigations (ultrasound,
MRI).
In this MRI of the ankle, plantar fasciitis, insertional tendinopathy with

thickening of the plantar fascia at heel level and deposition of calcium salts by
chondrocytes under stress stimuli and excessive traction (calcific enthesopathy)
are well known.
This is an ultrasound with PowerDoppler on where you

can see the insertion of the Achilles tendon, with an
irregular bone surface and inflammatory process that
incorporates the tendon and involves not so much the
bundles but the peritenonium. In this area there are
fatty pads rich in nerve endings and vessels.
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This is an MRI of the last phalanx of a finger where you can see a fairly large area of
bone edema.
Most common tendinopathy sites
These are the most common forms, but there are obviously much more. A high level center must be able to
correctly recognize all of them, and then send the patient to an appropriate treatment in relation to the
pathology and stage, in order to avoid the chronicization of the problem.
Infiltration therapy - Corticosteroids

They are useful in the short-term treatment of tendonopathies, in particular:
• Lateral epicondylitis (<8 weeks) [strong evidence]
• Tendinopathies of the lower limbs [moderate evidence]
• Rotator cuff tendonopathies [inconsistent effects]
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Injections with corticosteroids pose a serious clinical dilemma because, although their effectiveness has been
scientifically proven in the short term, tendinopathies do not have a real inflammatory pathogenesis; they are
effective only in the short term, reducing painful symptoms in the acute phase.
To minimize side effects, it is important that the infiltration is performed in the peritendinous region under
ultrasound guidance. If infiltration is made inside the tendon there is a risk of tendon rupture.
If an infiltration with corticosteroids must be done around the tendon, with low amounts of medication,
without repeating the maneuver several times. It has been widely shown that infiltrating with corticosteroids
around or even worse inside the tendon leads to apoptosis with consequent tendon injury.
It is also important to always investigate in pharmacological history the patient's intake of drugs that can cause
tendonopathies: for example, fluoroquinolones cause a tendon problem in about 30-35% of the population,
with various degrees of severity (symptomatology blurred or so important that the patient can no longer walk).
If treatment with the antibiotic is associated with a systemic corticosteroid the risk further increases.
And the problem can arise even for just a few days of therapy, even for one or two hires.
The teacher tells the case of a lady who took ciprofloxacin in the evening with the appearance of inability to
walk the following morning. After contacting the WYM, she took a second dose, with the appearance of painful
symptoms even when stopped around lunchtime. The GP then advised her to switch to levofloxacin, resulting
in a tendon rupture in the evening. Within 24-30 hours the lady broke the right tendon and severely
compromised the left one, after only 3 hires.
It is always essential to be careful and at the first signs to monitor patients with an ultrasound scan and stop
treatment.
Infiltration therapy with corticosteroids is burdened with multiple side effects:

• Tendon break
• Alterations in skin pigmentation
• Peritendinous soft tissue atrophy
• Atrophy of Kager's triangle, adipose bearing seen in the previous ultrasound scan
Due to the side effects and the short duration of action the use of cortisonics should be limited.
Infiltration therapy - Hyaluronic Acid

In studies conducted in patients with supraspinatus tendinopathy, epicondylitis and
insertional tendinopathy has been shown:
• Good functional recovery
• Reduction of painful symptoms
• Reducing disability
The infiltrative therapy with hyaluronic acid today represents the therapeutic innovation for tendon
pathologies. If the technique is well conducted, i.e. if it is performed under ultrasound guidance, if there is no
mechanical lesion of the tendon by the needle, if the type of hyaluronic acid is the most suitable (for tendons a
molecule of low molecular weight is chosen, between 530-1800kDa), the effect is mainly on the collagen
component and the endotenonium and peritenonium membranes. Hyaluronic acid, which we produce
physiologically, contributes to the lubrication and trophism of soft tissues and plays a fundamental role in
mediating the relationship between cell and water in the interstices. The water also makes it possible to lower
the temperature.
Hyaluronic acid is a molecule that is therefore able to retain water and make it interact with the cell (through
specific CD44, ICAM7 and ICAM6 receptors), and this biological mechanism means that even a tendon that is
overloaded during physical activity can maintain temperatures that are on average compatible with cell
viability.
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During a marathon, for example, after about 7-8km of running the Achilles tendon has an internal
temperature of about 40-41°C; after 10km it reaches 47°C and at this temperature all cells die, obviously also
in relation to the exposure time.
Possible therapies that provide the tendon with an instrument for lowering the temperature (such as water
linked to hyaluronic acid), promote the performance of sports activities that would otherwise inevitably lead to
compromise and tendon damage.
In the near future, many companies will start promoting hyaluronic acid infiltration therapies there. We were
the first in the world to do studies on these districts and we demonstrated all these aspects.
In this metanalysis 17 studies were compared, for a total of 1381 patients suffering from lateral epicondylitis,
treated with 8 different infiltrative therapies:
• Steroids (10 studies)
• Botulinum toxin (4 studies)
• PRP (2 studies)
• Hyaluronic acid (1 study)
• Prolotherapy, polydocanol, glucosaminoglycans (1 study)
PRP, prolotherapy and hyaluronic acid were the only medications that were superior to placebo. There is still
little evidence on what infiltrative approach to recommend for these patients.
Corticosteroids are effective, but it is so short that you only need to move the assessment to a longer follow-up
to lose the evidence.
Infiltration therapy - PRP

Plasma Rich Platelet PRP is done in an outpatient clinic by taking a sample from the patient himself. This is
centriguated, plasma and platelets are taken in a closed loop, placed in a tube containing calcium to activate the
platelets and finally injected into tendons or joints.
In the repair of mucosal lesions it has given extraordinary results, especially in dentistry, as well as in bone
regeneration in particularly delicate sites (insertional tendon diseases, avulsions with bone damage). It has
given rather good results when injected into joints or peritendinous tissues, especially with regard to painful
symptoms.
Infiltration therapy - Prolotherapy

Prolonotherapy, which is scarcely used in Italy, but more common practice in America, consists of sugar-based
infiltrations such as dextrose. This injection produces an inflammation which on the one hand causes intense
pain to the patient, on the other hand it follows a reparative process. This practice finds its rationale in the
observation in most cases of subacute inflammatory processes, protracted over time, which, when stimulated
and brought to a more vital, although more painful, condition, lead to a greater efficiency of the reparative
process with chronic resolution of symptoms. This practice is not shared unequivocally by all specialists, also
by virtue of the fact that the patient will not be able to benefit during this process of anti-inflammatory drugs to
reduce pain because it is in clear contrast to the rational above.
The professor affirms his personal opposition to this practice, stressing how its wider use in a health system
like the American one finds its reason in the low cost of this therapy compared to other options that he defines
from his point of view extremely more valid. To give an idea, he reports how the minimum cost of a vial of
hyaluronic acid is around €40 and up to an indicative maximum of €200 per cycle. Considering then that such
a therapy is prolonged chronically, at least until a hip or knee prosthesis is needed, the high costs of the
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treatment are clear, to which the costs of the medical service are added. In America, an injection of dextrose is
around $5.
Teacher's answer to a question (incomprehensible):

As far as hyaluronic acid therapy is concerned, two cycles per year are generally carried out with three
infiltrations each: one infiltration per week for three weeks is equal to one cycle followed by a follow-up
period. Clearly this is then also calibrated in relation to the clinical benefit that the patient reports. Obviously,
the addition of chondroitin sulphate background therapy and physical exercises with a good probability of not
needing any type of prosthesis over time should be emphasized in these cycles.
It is also interesting to note that PRP infiltrations have never proved to be superior to hyaluronic acid at the
joint level. So given the costs and problems of handling blood, he has always turned to hyaluronic acid.
One study reported that treatment with hyaluronic acid in patients with shoulder arthropathy, i.e. rotator cuff,
was the safest and most effective in comparison to the control group up to a period of 12 weeks; this against
the fact that exercise used in monotherapy was not as effective in the long term if not always associated with
infiltrative therapy.
It has been seen, in fact, that if one associates rehabilitative therapy, i.e. specific exercises included in the more
general concept of functional therapy, such as an eccentric activation of the supraspinatus to certain degrees of
abduction because those effective in that patient as representing the motor quota necessary to stimulate
biomechanically that tissue, to a pharmacological therapy on site, longer term biological effects are produced
that reduce painful symptoms. Returning to the previous example: carrying out a cycle of infiltrations to a
patient without associating it with any rehabilitative therapy is different from also providing specific exercises
for the knee (which aim at therapeutic objectives such as strengthening the quadriceps, lengthening the
structural, etc.) that in half an hour every day the patient will have to do for the first month, then every other
day for the second month and which will then be defined in a maintenance therapy that includes bi-weekly
exercises. In this way the benefit of infiltrative therapy lasts longer than 3-4 months without exercises,
followed by a window period of about two months until the next cycle when the patient feels pain again: the
combination therapy described above, on the other hand, manages to cover these two months as well. This
obviously has a not insignificant impact on the patient's perception of quality of life. This is clearly important
in order to allow the patient the normal continuation of his usual daily activities, which clearly has an influence
on the subject's motivational sphere, especially if elderly.
All this is clearly placed in a framework in which the approach of modern medicine and surgery in particular is
no longer the demolition approach, but the restorative and minimally invasive one. Suffice it to say that the
frequency with which menisci are removed today has been considerably reduced, also because it has been seen
that an intervention of this type was followed by a process of early arthrosis. In this context it is better
explained how an early approach, such as the one we are talking about, can preserve the quality of life of the
patient avoiding in many cases the need to use the prosthesis, with a simplification of the treatment for the
doctor and the post-operative for the patient who in this way could benefit the most from a minimally invasive
intervention.
High Volume Infiltration Therapy

High volume infiltrative therapy substantially affects pain. This study, called FULLY, examines a therapy in
chronic Achilles tendinopathy by adopting infiltrations with saline solutions, local anaesthetic and serine
protease inhibitors, with consequent anti-proteolytic action and reduction of the vasoactive effect. This type of
mixture in chronic innervating tendonopathies leads to a reduction in pain and improves function in the short
and long term, but increases the risk of adverse reactions if the cycle is repeated.
Mechanical-Functional Treatment
In this type of treatment, both intrinsic and extrinsic factors must be taken into account. In tendinopathies in
terms of therapy rationale, it is necessary to try to correct the misalignment of the osteo-musculo-skeletal
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component, compensate for joint instability, correct the muscle imbalances that may exist between agonists
and antagonists, strengthening the muscles.
As far as conservative treatment is concerned, rehabilitation uses exercises in which the eccentric exercise
component is particularly important as a therapeutic tool. The eccentric exercise involves active stretching of
the tendon muscle unit and in
particular the one involved in the
treatment of achilles tendinopathies.
The eccentric exercise, if prolonged
over time and dosed appropriately,
leads to a normalization of the tendon
structure with a reduction in
neovascularisation and a reduction in
the thickness of the tendon with
positive correlations also from the
ultrasound point of view: decrease in
hypoecogenic areas and fibrillar
degeneration.
In these pictures you can see an athlete doing an exercise that is partly eccentric and partly concentric, but
focused on the descent
(eccentric part). In the ascent
of the step the calf, then the
triceps of the sura and the
Achilles tendon, is shortening,
while in the slow descent
phase there is an elongation of
the whole tendon muscle unit.
This accumulation of elastic
energy is the basis for a
reparative process.
Usually the exercise is also carried out in the concentric phase, i.e. the ascent phase, with both limbs to further
reduce the concentric load on the tendon: then the descent phase is carried out with the diseased tendon only.
Dosages have been studied, as these exercises, if not protracted in time and specifically targeted to the
structure concerned, can be deleterious. This against strong evidence of tissue modification before and after the
correct treatment confirmed not only clinically but also in the ultrasound study. There is in fact a reduction in
the antero-posterior diameter of the tendon, a reduction in doppler positivity, an improvement in the fibrillar
structure that is more homogeneous with a decrease in areas of hypoecogenicity.
All this leads to the conclusion that mechanical conditioning can be used to heal the tendon. In fact, tendons
adapt to traction and therefore as a result of the load exerted by changing their structure and composition.
In a 2007 study, it was found that eccentric exercise significantly improves the outcome, hence the function,
and the painfulness of the patient with yarrow tendinopathy compared to a generic protocol exercise. In
particular, considering also the histological aspect, we have seen an increase in the synthesis of collagen,
especially type 1 collagen, with a reduction in its degradation, which leads to a progressive healing over time.
Therefore, the eccentric exercise has an impact on the length of the tendon: if the tendon is stretched its length
at rest is increased, progressively increasing the load on the tendon increases the intrinsic force of the tendon
and there is also an increase in the contraction speed which correlates with the greater developed force already
mentioned. Therefore the prerogatives and objectives of the eccentric exercise are to improve the elasticity and
therefore the length of the tendon, improve the load and therefore the intrinsic forces of the tendon and the
whole tendon muscle unit.
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As far as the dosage of this type of exercise is concerned, it is necessary to consider the speed with which it
must be carried out, the ideal load, the number of repetitions, the frequency and duration of the whole
treatment. This is also due to a necessary personalization of the protocol by virtue of the fact, for example, that
the patient is an amateur, amateur or professional athlete, or based on age, gender or even the quality of the
tendon itself.
Trying to think of a drug the load could be understood as the quantity, the number of repetitions as the number
of intakes etc.. The professor wants to emphasize the essentiality of understanding and operating this type of
treatment as a pharmacological therapy. For the latter, it will be the pharmaceutical company that will
provide this information, although the critical reasoning that leads to understanding how the same aspirin
tablet may have different efficacy in different subjects remains essential. This is to underline how similar
reasoning aimed at individualizing the most effective methodologies for the individual patient rather than for
another, also applying the concept of interindividual variability to these treatments. So it is the way the same
input is administered that drastically changes the outcome. Not to mention the many phenomena that must be
taken into account for a good vitality of the biological tissues: for example, one cannot ignore the atrophy that
muscles undergo in the bedding syndrome, not to mention the increase in bone mass resorption and the
reduction in the quality and coordination capacity of walking. It is clear from this that although these patients
are being given the best available therapies, sufficient in the case to resolve or control the main pathological
process, this is not the way to provide these patients with a qualitatively satisfactory return to their daily lives.
In short, the quality of medical care work not only passes from understanding the mechanisms that bind the
life of the cell to pharmacological, surgical or mechanical therapies (such as those being treated), but also
from understanding the context in which the patient lives on the basis of which to establish the best therapeutic
path that takes all this into account.
Alfredson Protocol
It includes a series of exercises so dosed: 15 repetitions x
3 series, performed 2 times a day every day, for 12 weeks.
The best results have been demonstrated by performing
the exercises on a platform inclined at 25°. This protocol
reported a result of around 88% in the Scandinavian
population (where it was tested for the first time, being
Alfredson of Swedish origin); however, repeated in other
populations (e.g. Mediterranean population) the result
drops to 65%: the orientation of the population influences
the result. However, there is no therapy for yarrow
tendinopathy that works better than eccentric therapy, not
even of a pharmacological nature.
N.B. It is interesting to note that a white man with a flat

foot is slow, while a black man with a flat foot has a flat foot that functions as a hollow foot, because the
quality of the connective tissue allows his foot to have an explosive gesture in the propulsive phase of the run
completely different from the white one.
Eccentric exercise
The concentric part of the exercise should be performed passively or with the
assistance of the contralateral limb (going up with one limb and down with
two), during the closed kinetic chain exercise (by definition, an exercise
during which the feet are bound to the ground, with muscle strength exerted by
the feet resting on the ground; in open kinetic chain exercise the foot is not
bound to the ground) reserving the eccentric phase to the affected limb.
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The eccentric phase consists of a single-podal squat downhill on a sloping platform. It should be performed
initially very slowly, and then increase the speed as the treatment progresses, always respecting the pain
(eccentric exercise is therapeutic if dosed at these levels, but if abused or maldosated it can be detrimental to
the musculotendinous unit, causing pathologies or tendon fractures).
Typically used for patellar tendon pathology, in the extension phase the extensor muscles of the knee are
activated and the tendon portion of the patellar tendon is shortened, in the descent phase the musculotendinous
component is lengthened, with accumulation of elastic energy in the intratendinous and myotendinous portion;
the result is a mechanical and biological therapeutic effect within the tendon structure.
This study shows the effectiveness of eccentric

exercise in lower limb tendinopathies in
athletes.
Compared to other therapeutic exercise models, eccentric

exercise in yarrow tendinopathy is more effective, resulting in reduced pain and swelling, patient satisfaction,
improved balance and proprioception (the quality of the tendon is the prerogative of elasticity, strength and
proprioception), improved agility, speed of return to activity and resistance in the dorsiflexion movement.
Study based on the comparison of patients who

have done eccentric exercises and patients who
have done concentric exercises; once again the
eccentric therapy shows superiority.
Epicondylitis, pathology of the extensor

muscle of the wrist. Generally,
peritendinous low molecular weight
hyaluronic acid infiltrative therapy, when
combined with eccentric exercise and
stretching with reinforcement of the wrist
and forearm muscle district, leads to a
better result.
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Rotator cuff tendinopathy

Pathology that mainly affects
athletes who use the shoulder to
perform specific sport gestures
(e.g. volleyball player, basketball
player, water polo player); it
frequently arises with age
(menopausal women). Eccentric
therapy.
In the treatment of patellar tendon

tendinopathy, concentric protocol
and eccentric protocol show equal
efficacy.
N.B. Often the patellar tendon

develops a tendinopathy that shows
fissures, lesions or calcifications
inside the tendon, so that the patient,
unable to perform the sport activity,
undergoes surgical treatment.
However, the patellar tendon
cleaning intervention in terms of effectiveness and recovery is not superior to the exercise protocol, which is
always attempted as a first approach.
Advantages of the eccentric

protocol in Yarrow
Tendinopathy and Patellar
Tendinopathy.
Eccentric exercise scheme

typically proposed: static pre-
and post-exercise stretching, 5
repetitions x 3 series of
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monopodalic squats increasing the speed during the week and associating at the end of each cryotherapy
training session; progression up to the 5-6th week, repeating the cycles and increasing weight and repetitions,
until the use of the eccentric isokinetic machine.
The machines used in rehabilitation are typically divided into isotonic and isokinetic machines. The former
are normally used in the gym, equipped with cables and involved in both the concentric and eccentric phases.
The second ones are connected to a computer allowing to know a constant (accommodating resistance) and
are particularly useful in the muscle strengthening enabling protocols, where the patient is asked to develop a
force starting from an already stretched muscle; in other words they allow the patient to express the maximum
muscle strength, because they do not behave like a leg extension (isotonic machine) because the more the
patient tends to extend the knee the more the machine resists.
A video is shown of a centre in Bologna that uses a neuromotor rehabilitation programme of movement
analysis after the reinforcement path. There is a screen where the athlete can watch himself performing specific
sport movements with a force plate, which is a vector that measures the reaction force of the ground; the
inclination of the angle between femur and tibia that is formed during the support of the foot on the ground
after a jump is an indication of the risk of developing a crusader injury. In the motion analysis, a motion
quality score is assigned, according to which a motor training program is set.
https://www.youtube.com/watch?v=CLp0eogoDNw
Physical Therapies
Cryotherapy is not a real

physical therapy, however it is
always useful to prescribe it in
patients suffering from
tendinopathy and muscle
injuries because it has positive
metabolic and physical effects
(e.g. reduction of blood flow and
swelling).
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HILT laser: high power laser, which

uses nd: YAG and penetrates deeper
than CO2 scanner laser. HILT laser
therapy is effective in improving
function, pain and quality of life in the
short and long term in patients with
lateral epicondylitis. It is generally
associated with infiltrative therapy or
exercise protocol.
According to some studies it seems that

electromagnetic fields have a
histological realignment effect on
collagen fibres, while low intensity
galvanic currents have no evidence
whatsoever.
Shock waves are a type of physical energy that uses hydroelectric, electrohydraulic or piezoelectric means of
regeneration. These are mechanical waves that interact with the underlying tissue (the photo shows the action
on the Achilles tendon) with a mechanotransducer effect: the acoustic mechanical wave impacts on the
pathological tissue inducing modifications on the tissue itself and activating cytokines, thus determining the
increase in vascularization, endothelium permeability and neoangiogenesis. They are significantly effective.
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N.B. the Veneto region passes a convention regime in the treatment with shock waves of plantar fasciitis and
calcific tendinopathy of the shoulder; in the case of yarrow tendinopathy and patellar tendinopathy the patient
must pay the hospital service.
From the x-rays shown it is possible to

observe the actual disappearance of
calcifications, however it would be
improper to define shock waves as a
physical means capable of allowing the
dissolution of calcium salts; rather they
induce modifications that help the body's
metabolism to reabsorb calcifications and
the healing effect is therefore evident.
The shock waves have an energy intensity

of 0.08-0.44 mJ/mm2. 3-5 sessions are
performed at regular one-week intervals.
Depending on the machine used, 1500-
2500 strokes per session are performed
visible on the display.
Shock waves have long been used in

the treatment of tendonopathies of the
lower limbs, proving to be particularly
effective in the short-term treatment of
non-insertional tendinopathy. In this
case they can be used as an alternative
to conservative laser treatment. They
are compared to closed-cell surgery,
because their mechanical-biological
effect (e.g. reabsorption of
calcifications) stimulates numerous
reparative processes, proving to be
effective especially when combined with rehabilitation therapy with eccentric protocol in tendonopathies.
N.B. shock waves have an extraordinary effectiveness, distinguishing themselves from many other physical
therapies (e.g. laser, ultrasound, electrotherapies, thermotherapies) which do not have great effectiveness;
naturally the effectiveness is amplified in association with therapeutic exercise.
PROTOCOL GENERALLY USED
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E.g. patient with non-insertional yarrow tendinopathy (i.e. in the body of the tendon): EO, ultrasound and
shock wave treatment associated with eccentric exercise; if the shock waves are not effective, we switch to
infiltrative therapy with hyaluronic acid. If there is an important picture of inflammation, a small amount of
steroids is administered once peritendinea-perially, before starting shockwave treatment or infiltrative
treatment.
A study in Padua led by Prof. Frizziero and a Belgian study compare the effectiveness of infiltrative therapy
compared to shock wave treatment, randomizing patients undergoing these treatments once a week for 3-4
weeks. It appears that the two treatments lead to the same results, although the infiltrative therapy is more
rapid in efficacy: the results are appreciable after about 10 days in infiltrative therapy, after about 30 days in
shock wave therapy; however, after these 30 days the efficacy curves overlap.
N.B. tendonopathies of large tendons (yarrow, patellar and rotator cuff tendonopathies) are always treated with
eccentric exercise, associated with infiltrative therapy or shock waves.
The physician, on the basis of

extensive biomechanical studies,
provides precise instructions on how
to construct the footbed, indicating
where the drain areas should be
located, where a certain type of
material should be used, in which area
the foot should be supported, the type
of cushioning on the heel, the way the
heel should be supported and the size
of the plantar vault. There are no
effective prefabricated insoles valid
for everyone: it is necessary to build a
specific footbed. The footbed does not
permanently correct the flat foot, but
only when you wear it.
In paediatric age, children with flat
feet are not initially treated in any way; it is only at the age of 6-7 years that the possibility of surgical
treatment or plantar treatment is evaluated.
The following is a series of slides about the pharmacological treatment, which Prof. B. does not dwell on,
underlining only the role of NSAIDs in tendonopathies, which are implicated only in synovitic forms.
15/10/2019
Castiglioni Giacomo Ginecologia, lesson 5
Benvegnù Francesco Prof. Ambrosini
DIABETES AND PREGNANCY

DIABETE
Diabetes is an insufficient secretion of insulin. A dysendocrine dismetabolic disease with an incidence of about
3-5 %. It can also be diagnosed during pregnancy with a low percentage of about 1-2%. It is a genetically
transmitted disease, but it also has non-genetic predisposing factors such as obesity.
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Components
The dysmetabolic component is hyperglycemia and ketoacidosis. But there's also a vasculopathic component,
which leads in the long run to microangiopathy.
CLASSIFICATION
The classification divides into type I, II, III and IV diabetes according to insulin dependence or non-insulin
dependence.
- Type I diabetes is an insulin-dependent diabetes mellitus and is a terrible juvenile onset diabetes.
There are also cases of very young children contracting this disease. These patients have difficulty
living a normal life: they are always walking around with the pump, they have to measure their blood
glucose several times a day, but especially in the long term they will develop a vasculopathy that will
lower their life expectancy.
- Then there is type II diabetes, present mainly in the elderly and not insulin dependent.
- Type III diabetes is the gestational diabetes that arises during pregnancy, it does not give vasculopathy
and dysmetabolism, but is still an important problem for mother and fetus.
- Finally, type IV or secondary diabetes is only a reduced tolerance to sugars. It arises in special
situations like Cushing's Syndrome.
CLASSIFICATION OF WHITE
[Professor reads slide]
Class A
 Reduced glucose tolerance demonstrated by altered glycemic values, but there are no clinical signs
Class B
 Presence of diabetes for less than 10 years
 Onset of diabetes after the 20th year of life
 There are no signs of angiopathy
Class C
 Duration of illness between 10 and 20 years
 Occurrence between 10 and 19 years
 No signs of angiopathy
Class D
 Presence of diabetes for more than 20 years
 Onset of diabetes before the age of 10 years old
 Signs of angiopathy
 Calcification of lower limb arteries
 Chronic hypertension
Then there are classes E, F, G, H [which the professor omits] and finally the R which presents malignant
retinopathy.
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DIABETES AND PREGNANCY
Any pregnancy is diabetogenic in itself, even with normal blood sugar or altered OGTT.
For type effects:
- Endocrine, with hormones that raise blood sugar like:
 HPL ( the most important)

 Cortisol
 Progesterone
 Glucagon
- Local
There is, in fact, a placental storage and consumption of insulin.
- Peripheral
Reduced peripheral tissue sensitivity to insulin.
So they're present throughout the pregnancy:
 Reduced glucose tolerance

 Increased cellular resistance to insulin
 Reductions in hepatic glycogen deposits
 Increased hepatic production of glycogen
GESTATIONAL DIABETES
It's only gestational diabetes that develops during pregnancy. A woman who has had gestational diabetes that
after some time develops diabetes, the latter is simply type I or II diabetes. It is a disease with relative
pancreatic insufficiency, but there is no vasculopathic component. Generally you have a return to normal after
childbirth. A blood glucose and an OGTT is carried out 8 weeks after delivery, in which the majority of
patients show normal values.
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DIAGNOSIS
It is diagnosed by measuring blood glucose, but in particular by performing an OGTT, in fact often the first is
normal while the second has values above the norm. Therefore, all pregnant women are given an oral glucose
load between the 24-28th week of pregnancy. First you make a glycaemia on an empty stomach, then you take
75 g of glucose and take the glycaemia after 60 min and after 120 min.
The reference ranges for pregnant women are:

-Fasting blood glucose
<91 mg/dl
-Glycemia after 60 minutes
<180 mg/dl
-Glycemia after 120 minutes
<153 mg/dl
In addition to this test should also be researched :

-glycosuria
-haemoglobin glycated
THERAPY
When the gynaecologist makes a diagnosis of gestational diabetes, the therapy is not his responsibility but that
of the antidiabetic centre, which in Padua is located at the Hospital Dei Colli. Most pregnant women solve this
simply with a proper diet. It is explained to the pregnant woman which foods to avoid, as patients often have
an unregulated diet. Also recommended is a low-calorie diet, with other types of sugars than those to which the
woman was previously accustomed. The diet is also rich in fat and protein and it is not uncommon for sugar to
normalize but for cholesterol and triglycerides to increase. For some women the diet is not sufficient to control
their blood sugar, so you have to give insulin which will most likely no longer be needed after giving birth. In
addition, during pregnancy the weight should be controlled: it is good to lose a few more calories by
accelerating the metabolism, making physical activity made especially for pregnant women.
FETAL MACROSOMY
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The highest risk of a pregnant woman with gestational diabetes is fetal macrosomy, i.e. a large fetus. You have
a birth weight above the 90th percentile and above 4200g.
Pathophysiology
Fetal macrosomy is caused by abnormal nutrition of the fetus due to maternal hyperglycemia. The result of this
is a fetal hyperinsulinemia which ultimately leads to increased nutrient use and thus increased growth. The
characteristics that the fetus presents are:
-alterated fat storage and distribution
-visceral hyperplasia
-accelerated skeletal development especially femur and shoulders.
Physiologically, baby mammals are proportionate to their mother's size. A woman of 1.50 m will most likely
have a child proportionate to her even though her father is an American basketball player, the child will grow
in height after being born. This mechanism saved us from fetal and maternal deaths.
So there are cases of tall mothers with gynoechoid pelvis who normally give birth to very large fetuses, even
up to 5 Kg. They are proportionate fetuses, which for all the different stages of pregnancy have been large,
which at the end of pregnancy still have considerable size and have therefore always respected their percentile.
Complications
It is different when a normal sized child becomes larger and very heavy due to unstable blood sugar, especially
when this happens in a normal or even small woman. Accurate measurements are taken of the femoral head
and belly and the computer can estimate the weight of the fetus, when it is above normal and the mother is
normal or small the risk is shoulder dystocia. In fact, the baby is able to start the labor from childbirth, choose
the upper and middle excavation, but then it gets stuck there, shoulders and belly can not pass. If the baby gets
stuck it dies, if you can pull it out by pulling it out it will suffer an injury to the brachial plexus and then a
paresis. Or another situation that can be created is that of a fetal suffering because childbirth becomes very
long and inquisitive and the baby will have a lack of oxygen to the brain for too long.
Treatment
The solution to this problem is an elective caesarean section, i.e. the baby is delivered on a predetermined day.
As the fetus is large, the delivery is not scheduled for the 40th week, but a little earlier. In Padua it happens a
few times to be at risk of shoulder dystocia, because all diabetic pregnant women are identified beforehand,
monitored and given birth in this way. The fetuses themselves are monitored ultrasonographically by
estimating fetal weight. This estimate varies by 20% compared to the actual weight. Knowing this variation in
case of doubt, it is always preferable to do an elective C-section in order not to take risks. The baby once born
is given a glycemic control, because the fetuses of mothers with decompensated glycemia during pregnancy
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can develop a kind of glucose dependence. These babies often faint after birth for a few days because they
have hypoglycemic crises, so they need to be monitored and monitored. They are used to living in a very
sugary environment and go into hypoglycemia very easily. We can see this phenomenon too: everyone is
always looking for sugar because as soon as it is ingested you have an instant feeling of well-being, the brain
starts to function well immediately, and you are accompanied by a sense of pleasure and satiety. It is also an
almost instantaneous source of energy but after a maximum of 3 hours hunger returns. The brain only
consumed sugar and is still asking for sugar. This is the same thing that happens to the baby.
Polidramnios
Finally, it should be remembered that the fetal macrosomy is also associated with Polidramnios , present in 6-
31% of pregnancies. It is related to poor glycemic control and has fetal polyuria.
PREGNANCY AND TYPE I DIABETES
Women who have type I diabetes are less fertile, especially when they are not on euglycemia. They are also at
risk of:
- Polidramnios
- IUGR or intrauterine growth restriction. The mother's microangiopathy affects the placenta, which
causes symptoms to the mother and in particular an arterial hypertension up to pre-eclampsia. Later,
the fetus will also suffer and develop incorrectly.
- untimely placental abruption
- premature birth (iatrogenic problem, it is the gynaecologist who induces the birth first).
- miscarriage due to malformations, in case of decompensated diabetes the risk is double that of a
healthy woman.
- fetal malformations, three times the risk in decompensated diabetes. In particular: cardiac, caudal
regression, spina bifida, anencephaly, anorectal atresia, renal anomalies.
- vaginal infections. Sugar changes the vaginal pH and the number of vaginal saprophytes. The most
typical is a mycosis.
- urinary infections
Type I diabetes complications
- Ketoacidosis, can lead to mental confusion and can be noticed with breath by the smell of fruit.
- Diabetic Retinopathy, can lead to a whole series of complications up to having to seek eye consultation
- Diabetic nephropathy, can lead to renal failure and increased maternal and fetal mortality.
[Prof. at this point resumes the discussion of how difficult it is to have a child with type I diabetes. Not so
much because of the problems with insulin therapy, but because of the awareness that your child will develop
serious problems in the long term due to vasculopathy. In connection with this, Prof. explains how in today's
medicine it is more and more complicated to communicate with patients because they get information on the
internet and then ask the doctor for too much explanation, accusing him of not having told them everything
they need. He concludes that it is difficult to tell a mother that her son will have serious illnesses due to type I
diabetes in 20 years, but the mother can still find this information with a simple click. All this, according to the
Prof., makes the work of the doctor much more difficult than in the past when he trusted the words of the
professional]
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Management
-Regulating diabetes before conception
-Control from the first trimester to avoid hypoglycemia and ketoacidosis, i.e.
 Regular diet and insulin therapy
 Regular meal times and snacks, because during pregnancy you eat little and often.
-Home blood glucose monitoring which must be maintained between 80-120 mg/100ml
-Monitoring HbA1c every 4-6 weeks
-induction preterm delivery if necessary. If the birth must take place before the 34th week, tocolytic drugs and
drugs that induce fetal maturity are used. In fact, surfactant production has not yet started and must therefore
be induced with an injection of corticosteroids. The problem is that both tocolytic drugs and corticosteroids are
hyperglycemic and therefore sometimes it is difficult to control the patient's blood glucose.
PREGNANCY AND TYPE II DIABETES
Care must be taken because many women are often unaware that they have type II diabetes, because while type
I has very obvious symptoms, type II can remain silent for longer and the symptoms can only appear late in
pregnancy. This happens particularly to women around the age of 40, who may suffer from glucose intolerance
and who become diabetic during pregnancy. These mothers' fetuses are at risk of fetal malformations.
Management
Before conception a diet must be made, which is prepared by the diabetologist or dietician. It is also
recommended to lose weight with exercise. Finally, in some cases insulin therapy is given to obtain
HbA1<7%, such therapy and glycated hemoglobin control can continue during pregnancy.
[A student's question: What happens to the fetus if a pregnant woman has a hypoglycemic crisis? Answer: If a
patient has a hypoglycemic or lipotimic crisis and faints, nothing happens to the child. Many pregnant women
happen to faint: the pressure during pregnancy is normally low and the consumption of sugar is very rapid,
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but the placenta has sufficient sugar and sufficient pressure to ensure the infant's blood supply of oxygen and
nutrients. The crisis usually lasts a few seconds. To avoid fainting pregnant women should do so very slowly
when they have to switch from sitting to standing position].
HYPERTENSION IN PREGNANCY, PRE-ECLAMPSIA AND ECLAMPSIA
HYPERTENSION DURING PREGNANCY
The phenomenon of hypertension in pregnancy is considered both for hypertension at the beginning of
pregnancy and for pregnant women who become hypertensive. Pregnancy, unfortunately, brings into play a
number of substances that can inherently promote hypertension.
1. A first example is that of progesterone:
- The increase in progesterone contrasts with the action of aldosterone on tubular sodium
resorption. It is known that progesterone rises a lot during pregnancy, especially during the first
few weeks (up to the 12th-20th week), which can lead to such an effect. It should be borne in
mind that this event can be induced both by progesterone produced independently by the pregnant
corpus luteum and by progesterone possibly administered by the gynaecologist up to the 12th
week, both in women with LPD (low progesteron disease) and in women of relatively advanced
age, for whom progesterone guarantees a more linear course of pregnancy.
 To preserve sodium, it increases the renin-angiotensin-aldosterone system. This

could strain the kidney itself, resulting in hypertension.
 Angiotensin would also be hypertensive, but placental prostanoids reduce

vascular sensitivity to angiotensin.
This phenomenon could therefore lead to a higher chance of having a higher than normal pressure.
2. The placenta, for its part, normally produces equivalent quantities of prostacycline, with vasodilator
and antiaggregating effect, and thromboxane, with vasoconstricting and aggregating effect. The end
result is a physiological balance. Imbalances in this system can promote hypertension.
3. Refractoriness to Angiotesin II, if it is not produced adequately, reduces vascular reactivity, increasing
peripheral resistance and consequently causing an increase in pressure.
To keep in mind is the following diagram:
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Gestational hypertension, if not compensated, can lead to pre-eclampsia and eclampsia. Similarly, chronic
hypertension, if not compensated, can lead first to pre-eclampsia and then to eclampsia. The difference
between the two branches of the scheme lies in the fact that while in chronic hypertension we are usually faced
with well compensated patients (because they have been on therapy for some time) but perhaps with a
cardiovascular system already compromised by years of illness, in gestational hypertension the cardiovascular
system is still "young" and performing. If, therefore, in this second case, we are able to maintain a normal
pressure with medication, the more difficult it is to have pre-eclampsia or eclampsia.
When it comes to gestational hypertension?
On the books it is written that gestational hypertension is defined as pressure > 140/90. In fact, already with a
pressure of 130/80 it is necessary to be alarmed, given the physiological hypotension of the healthy pregnant
woman. However, the fact remains that above 140/90 there is certainly transient gestational hypertension.
It is important to remember that gestational hypertension may remain the only alteration present, not
accompanied by proteinuria, resolving within 12 weeks of delivery and may or may not evolve towards pre-
eclampsia. You therefore have a situation that can be treated with the right therapy and that if well
compensated does not lead to major complications.
PRE-ECLAMPSY and ECLAMPSY
On the other hand, pre-eclampsia occurs when the pressure is greater than 140/90 and at the same time there is
proteinuria and a worsening of the general situation, given by the following factors:
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- Blood pressure > 160/110

- Decrease of platelets < 100,000 mm3
- Signs of renal distress from increased creatininemia > 1.2 mg/100ml
- Microangiopathy hemolysis
- Increased liver enzymes ALT or AST
- Persistent epigastric pain
- Headache or visual disturbances at an already higher level of danger
It is obvious that this happens very rarely, but this could happen in the worst cases.
If you get to ECLAMPSIA you also have convulsions, a sign of a situation already largely compromised. Of
course, such a situation should not only be managed during pregnancy and childbirth, but also during the
weeks after childbirth. The pressure should be monitored up to 3 months after the birth, and the pregnancy in
general up to 15 days after the birth, as convulsive episodes can occur even 15 days after the end of the
pregnancy.
CHRONIC HYPERTENSION
In this case we are dealing with a hypertensive pregnant woman, who knows her disease, or with a pregnant
woman at the second pregnancy who had developed hypertension during the first one. Basically, these patients
have a therapy already applied, which works well, and therefore leads to a normal blood pressure state.
The slide reads "diagnosed before 20 weeks": obviously we mean hypertension patients already before
pregnancy, not those who develop hypertension during pregnancy itself.
These pregnant women may, of course, also experience a worsening of their blood pressure situation, although
more rarely. These patients can show:
- Signs of kidney distress, with proteinuria > 300 mg/24h arising after 20 weeks.
- Sudden increase in proteinuria or hypertension or platelets before 20 weeks in pregnant women who
are already hypertensive and proteinuric. It is therefore necessary to check the proteinuria on 24h
already at the beginning of pregnancy and then every 3 weeks.
Such a general compromise will obviously be accompanied by a whole series of problems related to liver and
kidney failure.
What are the dangers of chronic hypertension?
 Preterm delivery (33%). When you have a maternal pathology in general you often have
pre-term delivery, since in most pregnancy pathologies "elimination" of the fetus blocks
the pathology.
 Superimposed pre-eclampsia (22%)
 Eclampsia
 Fetal growth defect (10%), because hypertension can lead to placental malfunction.
 Placental detachment (1-2%), linked to possible hypertensive peaks.
 Perinatal death (4.6%), linked not only to placental detachment but also to increased
mortality and morbidity in pre-term delivery.
 Maternal death (0.23%). This is the normal risk of emergency intervention.
Epidemiology of hypertension gravidarum
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As already mentioned, in Italy in general one does not die in childbirth. Very few women die, and almost
always from secondary causes. On the contrary, until 100 years ago, childbirth death was the first cause of
death for women.
Hypertension in pregnancy leads to over 50,000 maternal deaths per year, a figure to which developing
countries in particular contribute, where health is not well equipped. It is also the second leading cause of pre
and postnatal death, accounting for 20-25% of postnatal fetal deaths.
The mortality rate is more or less 1.5/100,000 pregnancies. In Italy there are about 500,000 births per year, too
few compared to the '60s and '70s, when the birth rate was over 1,000,000/year. A situation of this kind
confronts us with the "risk of extinction", considering the average of 1.3 children born per woman of
childbearing age (which is also affected by the positive contribution of the non-EU population). This is
obviously very much linked to the current working, economic, political, educational and relational reality. In
particular, the absence of policies aimed at fostering the creation of a family leads to an objective difficulty in
pushing the birth rate up.
In addition to these general considerations, the decrease in the number of children is also due to the individual
difficulty in accepting the change in life habits related to procreation.
In addition to this, it is important to point out that we are often faced with the obvious desire of the woman to
have a pregnancy, but this is hampered by the absence of the man willing to share this desire. If once the very
idea of a couple implied adherence to a "family program", today this no longer occurs.
Many of the prof's patients want a child in the absence of a partner, so they appeal to a sperm donor. Others
decide to have a child with another woman, a situation in which more and more often we see the stimulation of
one, donor fertilization and implantation in the other. Even men who wish to have a pregnancy can carry on
this wish, even if the situation is much more difficult and much more expensive. Finally, many women today
go into early menopause (POF = premature ovarian failure).
Resuming the discourse of the epidemiology of the hypertension gravidarum, it is observed that the mortality is
greater than 2-3 times in the black race. The black race, in fact, has more easily hypertension, hypertension
during pregnancy, gestosis, pre-eclampsia and eclampsia, uterine myomas. It is important to remember that
when we talk about the black race, we also understand African epidemiological data, unfortunately linked to
sub-optimal conditions in health systems. Mortality, finally, depends on pre-natal care. The example of the
USA is emblematic, and it is important to remember that basic care is not always guaranteed.
Anamnestic risk
- Smoking: smoking is always present, there is no disease in which smoking is not included in the
etiopathogenetic mechanisms.
- Twinship: A twin pregnancy exposes you to a higher risk of having polydramnios, diabetes,
hypetension etc.
- Previous pre-eclampsia
- Previous HELLP syndrome
Current risk
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As you can see from the slide, familiarity is important. More important, however, are chronic hypertension
and, to an even greater extent, the presence of chronic nephropathy. The presence of a nephropathy could lead
us to have to advise the patient not to carry out a second or third pregnancy if she already has a child.
RISK OF PRE-ECLAMPSIA IN RELATION TO THE NUMBER OF PARTS
Nullipares have a higher probability (3.9%) of having such problems than pluripares (second pregnancy ->
1.7%). If the interval between pregnancies is > 10 years, the risk is close to that of nullipares: it would
therefore seem that the number of children and the proximity between the parties reduces the risk of pre-
eclampsia.
FAMILITIES
There is a genetic predisposition to pre-eclampsia, and it seems that this is transmitted by both father and
mother, through genes that control the coagulation cascade, the lipid metabolism, etc..
The offspring of both sexes of pre-eclampic mothers have a higher risk of pre-eclampsia pregnancies, whether
it is directly the pregnant woman or the pregnant woman's partner.
METABOLIC SYNDROME 1 (Diabetes and Polycystic Ovary Syndrome)
In diabetes 1 the risk of pre-eclampsia varies from 9 to 66%, and obviously increases according to the classes
of White. This is because surely you will have already passed the stage of renal damage, therefore of
microalbuminuria, and of course you will not have any glycemic control.
In polycystic ovary damage (PCOs), which is a syndrome often linked to insulin resistance, naturally increases
the risk of suffering from gestational diabetes, hypertension and all those diseases related to these conditions:
gestosis, HELLP syndrome, pre-eclampsia, eclampsia. When you have a patient with diabetes or PCOs you
can therefore predict:
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- A more difficult pregnancy

- A more likely abortion
- A more complicated pregnancy
METABOLIC SYNDROME 2 (Dyslipidemia and obesity)
Patients with this type of problem must also be well monitored before the beginning of pregnancy and
especially during pregnancy. Having a patient who is obese or has cholesterol problems, we can predict that
pregnancy is likely to be more difficult.
Hypertriglyceridemia in the first half of pregnancy is a risk factor for early onset pre-eclampsia.
Obesity (BMI>29) increases the risk of gestational hypertension and pre-eclampsia.
Some characteristics of metabolic syndromes, therefore, lead to increased problems during pregnancy.
HEREDITARY COAGULOPATHIES
It is obvious that having a hereditary coagulopathy leads to a malfunction of the placenta and therefore a more
likely hypertensive state, resulting in kidney and liver damage.
The coagulopathies under examination are:
- Prothrombin deficiency III

- Protein deficiency C
- Protein deficiency S
- Leiden's factor V mutation
- High activity of the prothrombin, resulting from mutation of its gene
- Hyper-fibrinogenemia
- Hyperhomocysteinemia
In general, everything concerning the genetic mutations of the coagulation factors leads to a perfusion
difficulty and a possible placental problem.
What are the risks of hereditary coagulopathy?
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PRE-ECLAMPTIC SYNDROME
It is a syndrome that refers to a multi-organ problem, which includes several clinical manifestations in relation
to the target organs and is consequent to a generalized inflammatory state, similar to what occurs in tissue
oxygen debt. The major damage will obviously be to the kidney and liver.
These types of problems generally refer to the kidney, liver, s.n.c., lung and placenta. It is important to focus
mainly on the kidney, liver and placenta.
As far as the kidney is concerned, the reference pathological states are hypertension and proteinuria; for the
liver the HELLP syndrome, which we will see; for the s.n.c., the eclampsia convulsions; for the lung the
edema, in already advanced stages of the disease; for the placenta the I.U.G.R., a very particular pathology that
determines a reduced growth of the child in quantity and quality.
At the hemodynamic level you can have the following things (the prof reads the slide):
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Kidney:
83X
The kidney will naturally have glomerular damage, resulting in reduced glomerular filtrate and non-selective
proteinuria. In the most severe forms, creatininemia > 0.9 g/100ml may occur.
Liver:
- Fibrin deposition
- Increase in transaminases
- Periportal bleeding
- Undercapsular hemorrhages
- Epigastric bar pain as a clinical symptom
CNS:
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Cerebral edema, before convulsions, will cause headache and visual disturbances.
COAGULATION
The clotting problems concern the kidney and placenta. They lead to anatomical (microangiopathy), and
pressure (arteliolar spasm) consequences. All this leads to increased platelet consumption and activation of
coagulation factors. This vicious circle leads to renal dysfunction, in the context of which endothelial damage
is observed (which in turn leads to increased blood pressure), and placental alterations.
With regard to oxidative stress, it should be remembered that microcirculation damage together with oxidative
stress and endothelial damage lead to a general worsening of the initial cytotrophoblastic invasion. This leads
to an incorrect nesting of the villi, which do not fit well and are not perfusion correctly. Normally the
cytotrophoblast of the anchor villi colonizes the deciduous stroma and endometrial segment of the spiral
arteries early, disorganizing the muscular-elastic layers, reducing the vascular tone and ensuring low pressure
blood flow. If there is an inadequate cytotrophoblastic invasion, then there is a reshaping of the spiral arteries,
which stop working properly. This leads to placental ischemia, a state of oxidative stress, hypo-reperfusion of
intervillous spaces: overall you will have a badly functioning placenta, a fetus that absorbs less oxygen and
therefore grows incorrectly.
[I suggest you look at the slides for this part, since the professor reads successive slides without giving any
logical connection to the speech.]
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As can be seen from the image, in normal pregnancy there is an invasion of the middle third of the
myometrium: the villus enters up to this level. In the placentas that work badly, and therefore have incorrectly
inserted villi, there is an invasion limited to the endometrium: the villus, in this case, will die and stop working
well. It is therefore necessary for the villus to penetrate up to the myometrium so that it can perform its
functions correctly.
This type of patients are at risk of eclampsia, which may have the following characteristics:
- Blood pressure > 160/100

- Proteinuria 5 g/24h
- Risk of IUGR or oligohydramnios
- Diuresis < 500 ml/24h
- Risk of platelets
- Risk of increased creatininemia
- Risk of increased transaminase
- Risk of CNS malfunction, with edema (headache, visual disturbances)
- To the maximum degree, possible presence of pulmonary edema and convulsions
ECLAMPSY
In eclampsia, epileptiform accesses can occur before, during and after childbirth: it has already been said how
important it is to monitor the woman up to 15 days after childbirth.
In general, there are three periods:
The stage of tonic-clonic attacks can result in coma and death.
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HELLP SYNDROME
You have hemolytic anemia with microangiopathy. It can be recognized by a platelet and the exponential
increase in liver enzymes AST and ALT, which indicate liver damage. This damage is caused simultaneously
by endothelial lesions of the liver microcirculation, fibrin deposition in sinusoids, platelet consumption,
hemolysis with schistocytes and obstruction of the liver blood flow.
TREATMENT
GESTATIONAL HYPERTENSION THERAPY
Conceptually, hypertension therapy is delivery. If you are towards the end of your pregnancy and you fear
complications related to hypertension, it is therefore very smart to opt for the planned birth. If, on the contrary,
you are still in the first weeks of pregnancy, the decision is not so simple.
Therefore, if the placenta could not be removed, the best therapy would remain antihypertensive therapy.
To sum up, what are the maternal and fetal complications?
Fetal: the fetus grows badly, showing a difficulty of placental perfusion to Doppler flowmetry, causing an
increase in resistance at various levels.
Maternal: they are related to kidney problems (therefore with an increase in creatinine), liver problems
(increase in AST and ALT), problems related to platelets, anemia and uricemia.
The logic of the treatment lies in the correction of blood pressure linked to placental malfunction. The blood
pressure (the patient herself can do it) and proteinuria (every 15 days) of these patients should therefore be
monitored daily. At least every 15 days, they should then be evaluated clinically and sonographically.
When do we admit the patients?
You always resort to hospitalization when:
- you have a diastolic pressure in excess of 100 mmHG

- excessive proteinuria
- suspected fetal distress
PRE-ECLAMPSIA THERAPY
For the mother the medical therapy is antihypertensive (beta-blockers), while for the fetus resides in
cortisonics, to be used before the 34th week to stimulate the production of pulmonary surfactant. However, it is
important to remember how for both of them the moment of birth interrupts the pathophysiological chain that
determines the disease states. Childbirth obviously has to be managed according to the gestational era, after
having evaluated costs and benefits.
In the case of HELLP sdr prednisolone, which is the indicated therapy, has the function of prolonging the
pregnancy, without going to solve the problem.
Question: The slide reports that prednisolone cannot cross the placenta: but isn't it the same drug used to
stimulate the production of surfactant?
Answer: no, prednisolone is not the drug used to mature the lung.
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With regard to mild pre-eclampsia, it should be remembered that it is necessary to control fetal pressure and
growth, reserving the possibility of inducing labor after 37 weeks. The problem of severe pre-eclampsia is
precisely related to the fact that often it is not possible to prolong pregnancy until 37 weeks, and that
sometimes it is necessary to terminate the pregnancy earlier, to the detriment of the fetus, in order to protect
maternal health.
In the induction of childbirth, in general if the situation is stable you can even opt
for physiological vaginal delivery, while if complications are expected, a
caesarean section is necessary.
Zancanaro Elena
17-10-2019
Carofiglio Giuliana
Gynaecology lez. 6
Prof. Ambrosini
Natural childbirth and operational childbirth
In this table taken from a 16th century Medical textbook, the mechanism of childbirth was interpreted in an
imaginative and unreal way. The various presentations of childbirth are visible, some imaginative, others more
realistic. Not all parties take place with a summit presentation, as eutocentric parties, can take place in various
ways.
Currently the delivery mechanism is always understood as a "job" to be done using uterine contractile forces;
basically, without uterine contractile force, regular-vaginal delivery cannot take place.
Childbirth can be:
 Eutocic
 Dystocic
 Spontaneous
 Induced
 Driven
 Operative
 Simple
 Multiple
 Pre-term: <38 weeks
 Term: 38-41 weeks
 Post-term: >41 weeks; in most of the structures there is a tendency to give birth no later than 41 weeks
(Padua 41+3). This choice has no scientific basis, but is mainly due to a shortage of personnel. We try
to get women into early labor to avoid iatrogenic caesarean sections.
Childbirth occurs thanks to the rupture of the amniochorial membranes, the consequent uterine distension, a
phase of stress related to the release of cortisol by the adrenal glands, the activation of the hypothalamic-
adeno-neuro-pituitary axis as well as genetic factors, understood as predispositions to pregnancy-related
diseases.
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The stress phase, linked to uterine contractions, leads to a neuroendocrine activation that stimulates the
adrenals to produce cortisol; the contractions also lead the fetus to have to enter the birth canal. The birth canal
and its diameters are not so easy to pass, in fact, without a propulsive thrust from the uterus, without an
intelligent fetus capable of turning and without the proper size spontaneous birth cannot occur.
A synergistic situation must occur during childbirth:
 between the birth canal in the bone portion, then the pelvis, and soft: uterus, cervix and vagina
 between the movable body, therefore the fetus, active part in the delivery
 between the force of contractions
Labor is prodromal to childbirth, but it may or may not activate and if it does activate it is not necessarily prior.
If necessary, it can be pharmacologically induced. In labor you have:
 Increase in the number of receptors for oxytocin; oxytocin is the drug of choice to induce the onset of
contraction of uterine muscle fibres.
 Increased frequency of oxytocin secretion
 Formation of gap-junctions that allow the stretching of muscle fibres
 Oxytocin has a powerful pro-contracting action, mediated by the synthesis of PGF-2alpha by
amniochorial tissues; prostaglandins are other substances used for the induction of contractions.
 Coordination of contractions and onset of labor. In order for the contractions to have a laborious
effect and then allow the progression of the moving body, they must be coordinated, go from top to
bottom with a regular push and must also be regular over time. A simple contracture, with a sort of
uterine tetany, does not lead to fetal progression. The onset of labor is always linked to the onset of
contractions.
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Childbirth channel
The birth canal is composed of a bone channel, the small pelvis, divided into three floors: upper narrow,
middle narrow and lower narrow. They are three well delineated floors, with different diameters, but all
technically accessible by the normal fetus.
The upper strait is the entrance to the birth canal, the first strait with which the fetus is confronted. It extends
from the promontory towards the pubic symphysis. The medium strait has the largest diameter at the level of
the ischial spines, visible in horizontal projection. The lower strait extends between the pubic symphysis and
the coccyx. In the final push, which occurs when the fetus is in the lower strait, the coccyx plays a fundamental
role. It must be mobile, in fact a traumatized coccyx, therefore rigid after fracture, is not ideal for a
spontaneous delivery. At the last moment the coccyx must be extensible by about a couple of centimetres to
allow the diameter in question to be adjusted to avoid further fractures or prevent the fetus from leaving.
Important diameters can be found in the bone canal:
 Anatomical Conjugate: is the first step for the presented part of the child
 Midwife conjugate: it is a measure that can be found manually with a good approximation and allows
to find the anatomical conjugate, not measurable. The distance between the pubic symphysis and the
headland should be "measured" with the finger.
 Diagonal Conjugate
 Medium narrow: can be assessed by estimating the distance between the left and right ischial spines.
 Narrower: it is the smallest of the mentioned diameters, it becomes acceptable thanks to the
extensibility of the coccyx.
The birth canal also consists of soft parts: the lower uterine segment, the uterine neck, the vaginal canal, the
perineal muscle plane and the vulvar ring. These are soft, relaxing and elastic parts. The lower uterine segment
will be shortened and enlarged. The cervix, at its vote, will pass from a diameter of 0.5 mm to 10-11 cm, to
allow the fetus to pass. In contrast to the vagina, the perineal muscle plane and vulvar ring have lower
elasticity and stretchability, which is why they need maneuvers to reduce their tension in order to avoid
tearing.
Moving body
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The moving body is none other than the fetus, presented in most parts in fetal position and with the head
downwards. It is important to keep in mind both the diameters and the various skull bones of the fetus and the
small and large fontanelle, especially because by touching the sagittal line, the fontanelle, the bones, the root of
the nose or the mouth with your finger you can understand the presentation of the head. Not all babies who
have their heads down will have a normal position of the same, many have spoiled positions that tend not to
allow passage through the birth canal. The passage will be first the big parts, head, podice and trunk more
difficult, and then the small parts, upper and lower limbs.
Contractions
Contractions represent the "force" component of childbirth. They can be involuntary, peristaltic, intermittent
and painful (labor). The contractions indicative of the beginning of labor are rhythmic, occur every 15/10/5
minutes, and above all are painful. They are regulated by oxytocin,
which allows the depolarization of muscle fibrocells, lowering the
resting potential, with an increase in basal tone and speed of stimulus
conduction.
An auxiliary force component is the contraction of the maternal
abdominal press. In addition, the gynaecologist can perform
Kristeller's maneuver by applying a downward thrust, at the uterine
bottom, to facilitate the expulsion of the fetal head in the advanced
expulsive phase.
The first uterus in the figure is normal, weighs about 70 g and is about 7 cm long, with the cervix closed. On
the right are depicted the changes that occur during pregnancy, from the stretching of the uterine body to the
moment of contractions, when the uterine muscle fibres contract, the cervix shortens and flattens and the
cervix opens.
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Situation" means the relationship that is established, at the beginning of labour in childbirth, between the foetal
cephalopodalic axis and the longitudinal axis of the uterus. That is, the position of the fetus in relation to the
uterus, which is fixed in the longitudinal position. Therefore, there are two possible situations:
 Longitudinal situations.
 Transverse or oblique situations.
Cephalic presentations are all longitudinal situations. By cephalic presentation we mean that the first thing that
is ready to come out is the head, so it will be by longitudinal force. But also breech presentations are all
longitudinal situations because, in both situations, the fetal diameter of the breech-podal is parallel to the
longitudinal diameter of the uterus.
The shoulder presentation, on the other hand, is a transverse or oblique situation, it must be clearly modified as
it does not allow the exit from the birth canal.
By "attitude" we mean the relationship that is established, at the beginning of labour in childbirth, between the
various segments of the fetal body. In this sense they stand out:
 Total flexion attitudes: found in top and full breech presentations.
 Partial deflection attitudes: visible, to a greater or lesser extent, in all other presentations. The most
frequent are the presentation in front, incomplete and face, complete. In this case the head is not
flexed (chin towards the sternum), but deflected. The presentation of the first image is not optimal
because the diameter is large.
The fetal physiological attitude is that of total flexion or "egg-shaped" which offers the least resistance to
progression. The fetus will then perform rotations to find the best diameter to exit the birth canal.
The "presented part" is the first voluminous part of the fetal body facing the upper strait of the maternal pelvis.
Therefore, the possible presented parts are the head, the podice and the fetal shoulder. Then there can be lots of
mixes.
Cephalic presentations can be distinguished in:
 Bent presentation (best): complete vertex presentation, fetus with the head completely bent, and
incomplete presentation of Bremen or synclitis, in which the head is slightly raised.
 Deflected presentations: completely, face to face, or incompletely, in front.
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Each presentation has its own presentation index: when you go to touch the fetus' head with your finger you
can distinguish different bone structures, on the basis of which you can define the presentation index. In the
case of a vertex presentation, the occiput will be touched, in the case of a slight deflection (synclipsis) the
bregma will be touched, in case the head is even more deflected, then in the forehead presentation, the root of
the nose will be touched, in the case of the face presentation the chin and the mouth will be touched, in the
case of the podice the sacrum will be touched and in the case of the shoulder the acromion. This tactile
distinction between different anatomical structures is obviously not simple, it depends on experience, it is
facilitated by the help of ultrasound.
From the comparison between the presentation index and the point of finding of the mother's narrow superior,
the position (useful in the delivery room) is determined, acronyms are used to define the position of the
presented part.
OISA (Occipito-Iliac-Left-West) and OIDA (fetal occiput compared with right ileo-pettina eminence) are the
best: they refer to vertex presentations where the occiput is anterior and left or right, respectively. If the
occiput is posterior (OISP and OIDP) the situation is already more complex. In OISP the fetal occiput is
compared with left sacral sychondrosis and in OIDP it is compared with right sacroiliac sychondrosis.
(O=occiput, B=bregma, N=nose, M=sacre)
Childbirth periods
Cervical dilatation is measured in cm on the partogram: from 1 cm to a maximum of 10 cm which corresponds
to a complete dilatation. The uterine contractions discharge their maximum power from top to bottom in the
direction of the back wall of the uterus. Contractions have different dynamic effects in the two uterine
segments.
In the dilation period there are two phases:
- phase of preparation
- real dilation phase (with contractions occurring every 5 minutes with a duration ranging from 40 to 60
seconds).
This is the image of a gynaecologist inserting a finger into a vagina and feeling that the neck is still fully
preserved and not yet flattened. After that, it enters the external uterine orifice, runs through it and stops at the
internal uterine orifice, which is closed. The gynaecologist deduces that the neck is not yet prepared, but there
is a dilation of 1cm.
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This image instead represents a flattened neck with a 1 cm dilation and the opening of the internal uterine
orifice is appreciable. Cervical dilatation goes through a shortening and smoothing phase before starting the
actual cervical dilatation and forming the so-called "birth mouth". It is important to point out that in multipare
women it is common to find that cervix shortening and dilation can occur simultaneously and even more
quickly. The difference between the cervix of a multipara woman and a nullipara can already be seen from the
pap test: in fact, that of the nullipara will be long, cylindrical and completely closed, while that of the
multipara will look like the uterus. In fact, in multipare girls, complete dilation can be achieved even without
disappearing the neck.
Primiparenas have a longer labor, whereas in multiparent women, a shorter labor is expected.
During the dilating phase, amniorexi can be performed to allow the uterus to move into the fetal body and
make uterine contractions more effective in fetal progression in the birth canal. The gynaecologist has the
possibility to feel the bag, that is the balloon made by the stretching of the amnio-chorial membranes that,
when they break (the so-called "water rupture"), triggers the laborious effect that the rupture of the corial
membranes has. During this manoeuvre, possible compressions on the rope must be avoided.
At this point, the mechanical phenomena of childbirth are:
 reduction and commitment
 internal rotation
 progression
 disengagement
 external rotation or return movement
 deportation.
The head of the fetus must face the best diameter and place itself in the inlet part of the upper bone canal in
order to reduce its diameter. The intelligent fetus is the one that adapts by flexing, so as to reduce the diameter
of the head to fit into the canal. The fetus must also rotate to have an easy delivery, it must be able to confront
the occiput anteriorly, and when it is in the canal make an internal rotation so as to further decrease the
diameters. The time of the "internal rotation" allows the antero-posterior diameter of the fetal head to be
arranged along the antero-posterior diameter of the pelvic excavation, facilitating the progression of the head.
As it progresses and rotates, the fetal occiput moves below the pubic symphysis to the lower strait of the
maternal pelvis. Once the occiput has progressed to the pubic symphysis, pivoting on it, with a deflection
movement the disengagement of the head occurs.
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The Ritgen manoeuvre is carried out by protecting the perineum with the hand and following the delivery
movements, or with a towel. The aim is to protect the tissue between the vulvar host and the anus by avoiding
its tearing. The fetus' elbow during the passage can cause tearing.
In order to prevent the formation of decomposed lacerations, the gynaecologist can create sites of less
resistance by episiotomy. You cut skin, muscle and vagina with one cut of scissors. This is important then in
putting the episiotomy back in place: you have to sew up muscle with muscle, skin with skin and vagina with
vagina.
External rotation is important because it allows the shoulder to come out. You have to turn and not pull the
head, whose movement is followed by the exit of the front shoulder, back and finally the baby's ass. After the
removal of the shoulders there is no longer any impediment to the expulsion of the fetus.
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During shoulder disengagement, so-called "shoulder dystocia" may occur, which can cause serious injury to
the newborn. Such dystocia is more frequent in the presence of:
 maternal diabetes
 macrosomy
 obesity
 operational parts.
PLASTIC CHILDBIRTH PHENOMENA

Plastic phenomena of childbirth are two events:
 Head shaping: this is because the bones of the skull are still compressible and can be reduced by a
few millimeters.
 Childbirth cancer: imbibition of the presented part due to the difference between intra-amniotic and
external atmospheric pressure. It manifests itself with a more swollen and rounded head.
After expulsion of the fetus, the clamping of the rope and its section is carried out. Recently it is in vogue the
habit of clamping the rope when you no longer feel the pulse through it.
Another thing that has to happen after the expulsion of the fetus is the expulsion of the fetal attachments such
as the placenta, the chorionic membranes and the distal stump of the funiculus. This third period of childbirth
is called seconding and occurs spontaneously 10 minutes after expulsion; if it does not occur, it must be done
manually. With the explorer's hand you climb up along the cableway to the placental margin and then with the
ulnar side of the hand you disconnect the placenta chamfered from the underlying uterine wall. It is
recommended to perform the operation bimanually so as to avoid tearing or perforation of the uterine wall.
If the seconding does not occur spontaneously, the separation of the placenta can be facilitated by squeezing at
the Credè: facilitating the exit by causing pressure on the abdomen of the mother.
The term squeezing is not accidental: in fact "we must try not to push the uterine bottom down to avoid a
reversal of the puerperal uterus".
POST PARTUM
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All women who have given birth must remain

under control for the next 2 hours after expulsion.
You have to check their parameters (pulse and
pressure), and the contracture of the uterus
(bottom of the uterus, oxytocinic drugs, any
bleeding).
OPERATING PARTS
For many years, the terminology "operative birth"

was mainly understood to mean the application of
forceps, and for a long time almost every
obstetrician had "his own forceps" built.
Classically, the various types of forceps can be
distinguished into 'parallel-branched forceps' or 'superimposed-branched forceps'.
The forceps is a tool that allows you to take the child's head deep, where you do not reach with your hands,
making a smart rotation. The conditions allowing the application of forceps are:
 full expansion
 absence of fetal-pelvic disproportion
 fetal head deeply involved in pelvic excavation
 broken chorio-amniotic membranes
 fetus alive (if the fetus had died, it would have detached its head by maceration).
The actions of the forceps are:

- rotating action (once the fetus' head is grasped, it must be rotated)
- reducing action (by bringing the bones of the head closer together, the diameter of the head is
reduced)
- pulling action.
In conclusion, the forceps performs two actions which should occur physiologically; the lack of these requires
the use of this instrument. We're talking about:
1) reducing action, which the intelligent fetus should perform in order to enter the channel
2) substitution of the force that would have been required from the contractions for the expulsion of
the fetus.
There is another tool used in addition to forceps: the obstetric suction cup. This is applied to the child's head, is
shaped like a cup and in contact with the skin creates a vacuum (like a sort of suction cup) so that it can no
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longer be detached from the child's head; thanks to these features it allows you to make a traction. An incorrect
application at the height of the fontanelle creates serious damage to the underlying brain structures.
CAESAREAN SECTIONING TIME

The C-section is not a difficult operation but requires experience to perform it. Moreover, it is extremely
emotional because it often occurs in emergency situations; no less it takes place in conditions that can be
vulgarly defined as "dirty" (e.g. failure to empty the intestine, bleeding, amniotic fluid leaking), and many
gynaecologists have fainted in the operating room. It's done:
 a transverse incision on the lower uterine segment creating the so-called uterine breach. It cuts the
skin, the subcutaneous with fat, the fascia with muscles. Initially the parietal peritoneum is opened,
followed by the visceral peritoneum. Above this is the bladder, which is lowered, thus finding us in
front of the uterine cavity. If the cut is wrong, which should only be made on the lower segment
(because the abdominal muscles are very powerful), a large amount of blood comes out and the
delivery is complicated.
Performing a C-section on a woman in labor is much easier because the lower uterine segment is in
this case already "ready", i.e. stretched and thinned. Once you insert your arm into the uterine cavity
to grab the fetus, the uterus will tend to close and sometimes it is necessary to make an additional "T"
cut in order to have more space. In gynaecology it is very important to be as gentle as possible.
 digital enlargement of the uterine wall with L-shaped pliers
 extraction of the fetus by ascending along the stump of the umbilical cord; in this way the placental
Giovanni Zenari
margin is reached and the placenta is detached manually. 22/10/2019
Giovanna Bazzolo
 the uterine breach is cleaned and closed by recomposing the visceral peritoneum Gynaecology lez. 7 of
with repositioning
Vasco the
Cazzagon Prof. Ambrosini
bladder; the parietal peritoneum is then recomposed, followed by the reconstruction of the fascia,
the stitching of the right muscles, adipose tissue and skin.
[Integrated lesson with last year's uncoils]
During the previous lesson we dealt with eutocentric delivery, a delivery that is not particularly difficult, a
natural delivery, with the top presentation, i.e. where the head is the first part that goes out. This is a birth
with which most newborns are born (95-97%) and represents the type of delivery with the least complications.
DISTOCIES and ANOMAL PRESENTATIONS
Today, through the tools that allow us to know in advance the possible problems and available surgical
interventions, delivery in the presence of dystocia is a delivery that can normally be resolved without
complications. In the past, this type of birth had one of the major causes of death of the mother and the fetus.
Even when the fetus was able to come out very often there were problems a posteriori, such as mental
retardation in children, caused by suffering from childbirth, a lack of oxygenation for a more or less long
period. Today this kind of problems are no longer found in term children but sometimes they are found in
children born prematurely (until 30 years ago there was no neonatology so children born at 23-25 weeks were
not resuscitated).
The anomalous presentations are those that are not at the top and concern 3-5% of the parties; now it is
possible to foresee them and limit the problems.
Definition of dystocia: any abnormality of labour in childbirth. Depending on whether it concerns the
mechanical or dynamic phenomena of childbirth, a distinction is made:
- Mechanical dystocia: from lack of engagement or progression; the fetus is unable to engage the
pelvic excavation and progress towards the vagina. For example, for large fetal sizes;
- dynamic dystociae: they present problems with contractions or dilatation of the cervical canal; for
example, thrusts and contractions are missing.
For the general diagnosis: you put a finger in the vagina and see the type of presentation (the so-called fetal
index).
Abnormal Presentations
Abnormal presentations can be:
- cephalic presentations (syncope, forehead, face), 1%;
- shoulder presentations, <0.1-0.2%;
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- breech presentations (complete variety, buttock or frank variety, foot variety, knee variety, mixed
varieties), 2-3%.
The ideal situation is that the head is very flexed; in other cases, especially after a long labour (up to 10-24-48
hours) the head of the newborn will present a typical "delivery tumour".
Cephalic presentations
A distinction is made between partially deflected cephalic and deflected presentations. (Editor's note. The
cephalic presentation is classified according to the degree of flexion of the head with respect to the fetus'
body: generally the degree of flexion is maximum, with the fetus' chin in direct contact with the chest  vertex
presentation. Source: Core Curriculum Gynaecology and Obstetrics, Ferrari and Frigerio).
Partially deflected
presentations
Presentation of Bremen or Syncipite. The skull is in incomplete flexion, partially
deflected; this presentation is often unstable and is likely to change into another
cephalic presentation during labour in childbirth (therefore one could go so far as to
have a vertex presentation and thus have a normal delivery or one could go so far as to
complicate a more deflected presentation). If it remains stable, it allows natural
childbirth often with sacral rotation of the occiput, then the fetus will be brought out
with its face upwards. This rotation is given by the attempt to find a diameter that
allows the head to pass from the middle excavation to the bottom. In any case, the
expulsion period is considerably longer.
Diagnosis: complete perception of the bregmatic fontanelle and sometimes of the small
fontanelle; after childbirth by evaluating the typical delivery tumour (see image
opposite).
Risk: the risk that this type of delivery involves is that of secondary uterine hypokinesia because when the
labor is very long the tired uterus can no longer contract; even the drugs that act at the level of those fibers and
receptors are not able to have the same effectiveness.
Deflected presentations
Presentation in front. Also called incomplete or unstable, because it can change during labour. It has a
frequency of 1/1000 travails.
The fetal index is the root of the nose, while the cephalic diameter that compares with the birth canal is the
sub-occipito-mental one (13 cm). Obviously it is more problematic the term fetus of 38 weeks, which will be
very large; in the case of a fetus of 32 weeks the problem does not exist because the spaces are so large that the
situation solves itself.
It usually resolves: the baby turns over, the head bends and the birth occurs
spontaneously. This happens because the fetus feels the contractions and being in a
difficult position it turns and moves as if it has a natural predisposition to find the right
presentation. If the baby does not turn around, delivery by natural routes is generally
not possible because the maximum diameter of the fetal head (occipito-mental =13.5
cm.), which is incompatible with any maternal pelvic diameter, oscillates in the
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excavation. So, normally, when you recognize a presentation in front of you, you leave a limited time to the
fetus to turn around, but if this does not happen, you proceed with a caesarean section.
At birth the newborn baby may present the typical delivery tumor shown in the figure, which is not worrying.
Face presentation. Also called complete or stable (does not resolve
itself). The deflection is complete with the occiput in contact with the
back. It has a frequency of 1/400 travails.
The fetal index is the chin and the most frequent form the "chin-right-
posterior". The cephalic diameter that engages in the birth canal is the
fronto-menton (9.5 cm); this means that it passes the upper excavation
but stops at the middle.
So the main problem with this presentation is that the fetus manages
to enter the birth canal but then fails to turn. The critical time is that
of internal rotation, where the chin rotates anteriorly and is carried
under the pubic symphysis. This does not happen and in the pelvic
excavation a composite diameter (sterno-sincipital = 17-18cm) is
found absolutely incompatible with any pelvic diameter.
Vaginal delivery is therefore risky, it is better to do a C-section
directly. The great obstetricians of the past were able to do this, had
more experience and were more serene, without the burden of
medical-legal attacks, in dealing with natural parts in abnormal
positions.
Assuming that the child is able to get out (this can happen if the child
is small for the pelvis), the disengagement of the head occurs without
difficulty through a bending movement, exactly the opposite of what
happens in vertex presentation. Instead of pulling it up, you pull it down. If the head is
gone, the rest of the delivery will go more smoothly.
The newborn will present the typical tumor, larger than the presentation in front, and
in addition:
- facial swelling;
- bruising;
- deformation of the features, with oedema of the eyes and nose;
- persistent deflection attitude in the first few days.
Presentation of shoulders
It is a rare oblique or transverse situation, with a
frequency of 1/200 travails (in the past it was more frequent because
it was typical of large multipares). The Professor (fortunately
for him) never had one.
There are some predisposing factors:
o multiparity;
o uterus septum;
o voluminous myoma;
o placenta previa;
o polydramnios;
o prematurity;
o twinship.
The presentation index is the acromion, very difficult to distinguish on palpation.
The undertaking given by the party submitted is impossible and is therefore an elective indication of
Caesarean section.
Risks: PROM, i.e. the premature opening of the chorionic membranes with the liquid that descending can exert
pressure on other structures causing them to protrude downwards. Almost always occurs the anterior prolapse
of the rope and in some cases the descent of an upper limb which then has to be repositioned inside.
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Breech presentation
This is a longitudinal situation. Although it has a low frequency (2-3%), it is the second presentation by
frequency after the top one.
In the past, when it was understood that the presentation of the fetus was breech, Leopold's maneuvers were
done, trying to rotate the fetus, although they often did not work and indeed there was a risk of uterus rupture.
Very often these were fetuses that were not born, remained there, became infected and gave septic shock with
death even of the mother. Nowadays it is no longer worth doing a turning manoeuvre or a breech delivery,
there is a tendency to do a caesarean section. The professor says that it is almost easier to perform a C-
section in the case of a child in breech presentation than one in cephalic presentation.
The index of presentation is the sacred for which 4 starting positions are recognized: SISA where the sacred is
presented anteriorly and a little to the left, SIDA, SISP and SIDP. But the starting position is of little relevance
for the subsequent delivery mechanism. Again, there are some predisposing factors:
o prematurity. This happens because the fetus spontaneously tends to turn around to assume a cephalic
presentation during pregnancy; in fact, the frequency of breech presentation decreases with
increasing weeks of gestation: 25% under 28th sg, 7% at 32nd sg and 3-4% at term. Source:
Gynaecology and Obstetrics, Zanoio, Barcelona and Zacchè);
o twinship;
o uterine and placental abnormalities;
o pelvic abnormalities.
Different varieties are recognized depending on the
fetus' more or less flexing attitude and depending
on which part comes out first:
 complete or frank (15%) (fetus on the
left): buttocks only, and it's the best;
 incomplete (fetus on the right): buttocks,
feet, knees, mixed. They're more
problematic.
Leopold's maneuver: If there is a persistent

breech presentation at 37-38 weeks it is possible to
perform the obstetric maneuver of external reversal. This manoeuvre must be carried out by two operators
and has a success rate of 50%, which is lower in primipares, Caucasian women, in the case of committed
podice or obese patients. The risk of recurrence is in any case 3%, i.e. when the membranes rupture, the child
has returned to the breech position. It is carried out under ultrasound guidance to identify the baby's belly and
back curve and provides for forward rotation of the fetus; during the manoeuvre it is necessary to monitor the
fetal parameters. It is not risk-free because it can lead to a rupture of the uterus and is contraindicated in case
of:
 previous hysterotomy;
 placenta previa;
 p-PROM: there is already a leak of liquid where for a
successful manoeuvre it is essential that there is a
"bubble of liquid", otherwise the child sticks and it is
impossible to move it;
 oligoamnios;
 IUGR;
 uterine malformations;
 maternal pathologies: chronic and gestational
hypertension, heart disease.
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Parentheses on the placenta previa (from last year's uncoil). The term placenta previa means a very low
placenta near the internal uterine orifice. It can be complete if it completely covers this orifice or marginal,
more or less close (2-3cm) to the orifice. Usually the placenta is located either on the front or the rear portion
of the uterus, but in a high position, towards the bottom.
This is a pathology (which we will see) that usually resolves well because the uterus dilates and causes the
placenta to detach, but causing bleeding that can frighten the woman.
A marginal placenta previa could be compatible with spontaneous delivery, while a complete placenta previa
placed in front of the orifice would not allow natural delivery.
The cesarean section of a prior anterior placenta is complex because once the uterine segment is opened you
are in front of the placenta with the need to pierce it and consequent bleeding. The posterior placenta previa is
not a problem.
Childbirth takes place according to the usual 6 times, with direct reduction by compression of the soft parts and
internal rotation; i.e. the fetus turns, turns and descends. The disengagement of the podice is achieved by
lateroflexion of the back until the anterior hip is under the pubic symphysis and facilitates the disengagement
of the posterior buttock and then the anterior buttock. So the pubis acts as a pivot and allows him to lower the
rear buttock coming out and then the front one coming out as well. It is easier to disengage the back than the
front because the latter, whether it is a shoulder or a hip, can get stuck in the pubic symphysis.
The fetus descends quite easily due to the fact that the buttocks, although having a large diameter, are easily
compressible; the big problem of breech birth is the impossibility to predict whether the shoulders and the head
will be able to pass.
In the buttocks or frank variant the progression of the presented part can be made
difficult by the slatted effect that the legs extended on the thighs could carry out; i.e.
when the legs are straight (see picture on the side). This makes it more difficult to
rotate the shoulders and then the head.
It would be preferable to have a flexed leg because it would give you a chance to go
and take your foot out in the meantime.
At this point for the assistance in breech birth of the
buttocks or frank variety you can perform the Bracht method (picture on the left)
which consists of crushing the lower limbs of the fetus against the abdomen and all
against the mother's belly until the fetus overturns. You always think the fetus has to
do a flip.
Once the podice has been ejected, it is

possible to facilitate the ejection of the lower
limbs by performing the accompanying
manoeuvres always and only during
contractions in order to avoid "limb barrages"
(see image on the right). A typical maneuver is to place the fingers in
front of the hips of the fetus, it is better to use both fingers because one
with only one finger runs the risk of fracture of the hip. This manoeuvre
helps to get a better grip on the child that would otherwise tend to slip
away. Another maneuver that is quite trivial is to move the baby's ass to
one side when trying to free the opposite leg. The moment you have to
pull out your upper limbs: you enter with your hand, let one arm out,
turn around, let the other arm out.
And finally the head comes out: it is the most difficult moment because
almost always in the baby it is bigger than the buttocks.
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Mauriceau- Veit's manoeuvre (bottom right image) which consists in placing

a finger in the baby's mouth (unless
there is fetal suffering you can hear
the baby sucking your finger)
helping him/her to flex his/her head
in this way, because in this way the
chin is pulled down, making the
baby do a "somersault" towards the
mother's belly. Even in the
Caesarean section it is possible to
use this maneuver in cases where it
is difficult to pull out the head.
One of the most feared and most frequent complications of breech birth is the
limb barrier, where practically the fetus has the limbs behind the head.
Usually of iatrogenic origin: often because of the hurry the child is pulled too soon. Pulling the child before the
exit of the shoulders will cause the shoulders to rise and prevent the next descent. Before making any
maneuver to reduce the limb barrages, it is necessary to understand how the limb barrage is placed:
 "by ascent" (first image on the right) where the barrier
can be solved either by autonomous movement of the
fetus or by inserting the hand and helping it;
 "by descent or retronucal" (second image).
To recognize the type of weir it is useful to evaluate whether the
axillary cable is closed or open.
Weir reduction manoeuvres

The only thing to do is to enter with 1 or 2 fingers, try to
understand how the limb is positioned, follow it until you
find the elbow and pull it down. Usually by applying light
pressure on the inner corner of the elbow the fetus will
respond by bending the limb and this gimmick can
facilitate the exit. Such maneuvers are somewhat
improvised, based on the situation and intuition of the
doctor.
The rotation and slight traction of the fetus can also help
to solve the barrier.
In the past, they even used to cut the pubic bone. Then going to give the
mother a great deal of pain after the birth.
During breech extraction manoeuvres the grip must always be solid, two
hands firmly on the buttocks, because it is important that there is traction. So
the obstetrician must be strong because it takes a little strength but also
gentle to not create trauma or fractures.
You have to position your thumbs upwards so that you have a more secure
grip and since the little body is covered with blood, amniotic fluid and
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caseous paint1, a kind of slimy cream that makes the fetus' grip particularly difficult. It may be useful to help
yourself with a sterile towel or to clean it or use the towel itself to hold the baby.
The professor cites examples of clinical cases that have happened to him in the course of his profession:
 Case of a dead fetus intrauterus and now macerated, which was "decapitated" in an attempt to get it
out of the birth canal,
 case of fetus with diffuse anasarca (edema diffused to the whole body), stuck in the birth canal and
therefore dead.
The Caesarean section in natural delivery body is successful in case of positioning the head in the pubic
excavation; in this way, through rotary maneuvers of the fetus, it can be extracted. In the case of the delivery
channel with abnormal presentations, even with a Caesarean section it is difficult to extract it (very
disconnected and unclear speech).
The important thing for the gynaecologist is not to find oneself in the situation of not being able to do anything
any more, not least because of the many legal problems one may encounter.
He cites as an example of how in the past all the medical-legal aspects were not as relevant as today the first
echo-guided amniocentesis in Padua, in the 60s: given the poor resolution of the machine, the amniocentesis
needle had penetrated the child's heart. This was not followed by any legal action.
He returns to the usual discourse of the change in the doctor-patient relationship compared to past decades,
adding that today, in order to protect himself from legal action, the doctor must strictly adhere to the
guidelines and therefore is somehow "limited" in his action.
LABOR MONITORING
Birth can now be monitored in order to see the state of the fetus, i.e. whether the fetus is well. Travail
monitoring, i.e., indicates all methods of monitoring fetal well-being during labour.
The classical methods of assessment of fetal conditions are:
 BIOCHEMICAL MONITORING
Indicates the fetal blood test for the evaluation of:
 Blood pH,
 acid-base balance,
and is traditionally carried out by means of a Saling technique, i.e. micro-pick-ups of blood from the
scalp of the fetus, through the vaginal canal, on which hemogasanalysis is then performed. Only
possible in case of broken membranes.
The most recent method of biochemical monitoring is the PULSED OXIMETRY which consists of
continuous trans-cutaneous measurement of fetal blood oxygen saturation.
From the slides, it indicates the continuous trans-cutaneous oxygen measurement of fetal blood, whose
normal value is FSpO2 > 30%.
Through this monitoring method, the blood pH, pCO2 and BE values are known, from which it is possible to
establish the type and extent of any acidemia present (remember that in the fetus hypoxia determines FIRST
respiratory acidosis and POI, with activation of anaerobic glycolysis, metabolic acidosis).
1
Editor's note. Caseous varnish: fat material incorporating fragments of epidermal cells, shiny and yellowish-white
in appearance, which covers the skin of the fetus, protecting it from maceration by the amniotic fluid in intrauterine
life.
104X
It is a relatively little used method.

With regard to the pH-meter in labor in childbirth:
 values > 7.25 are normal,
 values between 7.20 and 7.25 indicate the need to repeat the examination on the basis of
cardiotocographic trace, colour of LA and risk factors,
 values < 7.20 indicate the need to carry out the birth in a short time.
If low pH and signs of fetal distress are present, the doctor should terminate the pregnancy:
- If the uterus is well-contractile, fully dilated and the lower strait band is in place, the fetus will have to
be extracted quickly using instruments such as a suction cup or forceps,
- in case there are no such conditions and the fetus is still "high" I have immediate indication for
caesarean section.
Therefore, in case of indications of fetal distress, either the natural childbirth is accelerated, or you go to the
operating room to perform the Caesarean section.
Micro-abstraction of blood from the fetal Pulsed Oximetry

scalp
 ELECTRONIC MONITORING
Indicates cardiotocography (direct or indirect):
 uterine contractions,
 fetal heart rate.
CARDIOTOCOGRAPHY
Allows the evaluation of

 heart rate,
 uterine contractions during delivery.
[Definition according to Wikipedia: a widely used obstetrics exam to assess the well-being of the fetus in the
perinatal area and the presence, frequency and extent of contractions of the mother's uterus during delivery].
The parameters to evaluate the cardiotocographic trace are:
 Baseline,
 variability:
- in the long term (during all labor),
- in the short term (during the last half hour of labour, for example)
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 changes in the baseline, i.e. fetal heart rate, which can be accelerations or decelerations,
 contractile activity it is important to check whether the accelerations and decelerations are in
correspondence with the contractile activity.
Normal baseline characteristics:

- 110-160 bpm,
- Recording of at least 10 minutes or less does not allow sufficient information to be obtained,
e.g. to check for frequency accelerations or decelerations,
- absence of periodic or episodic changes a fetus with flat trace is a fetus that does not move,
- sympathetic activity causes an increase in frequency, parasympathetic activity causes a reduction
in frequency.
Fetal tachycardia
May be
- slight 160-180 bpm,
- severe > 180 bpm.
Causes are:
- anemia,
- infections,
- medicines
Fetal bradycardia
May be
- slight 100-110 bpm,
- severe < 100 bpm.
Causes are
- conduction defects,
- Compression of the most worrying
complication, usually occurs by crushing
between the fetus' head and the birth canal,
- idiopathic.
Baseline Variability
The heartbeat varies by fetal response, i.e. according to what the fetus does;
(long term: 1 minute for 5-20 bpm, 2-6 fluctuations)
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The heart rate can be recorded directly (from the fetal scalp, by directly applying a spiral electrode) or
indirectly (through the maternal abdomen, using the Doppler effect).
It reiterates how important it is that there is variability in the track, because a completely flat line is an
indication of fetal distress.
(short term: computerized, beat-beat, 6-10 bpm).
Increased baseline variability indicates a rapid increase in the fluctuation
above 25 bpm; the pattern is referred to as "jumping" and is due to
excessive parasympathetic activity:
- response to hypoxia,
- vagal stimulation by head compression.
It may be associated with variable decelerations (ups and downs, with

accelerations and decelerations).
Reduced baseline variation indicates reduction below 5 bpm,

with minimal acceleration and deceleration. It is an alarm
signal, it indicates that the delivery must be completed
quickly. However, it will be a complicated procedure because
there will be no help from the mother, which means that
uterine contractions will be very little need for a caesarean
section.
Causes are:
- sleep (lasting 15-30 minutes),
- quiet,
- drugs,
- prematurity,
- neurological abnormalities,
- fetal acidosis.
The heart rate therefore has a periodicity that reflects the fetal response to stimulations, which cause
accelerations and decelerations. However, these must be around a regular baseline (110-160 bpm);
Accelerations increase in frequency by at least 15 bpm for

at least 15 seconds; they are divided into:
1. sporadic, unrelated to uterine activity, reflect fetal
movements,
2. periodical, uterine-related and dependent on fetal
movements and cable compression.
There are different types of heart rate, contractions,

contraction-frequency correlations the tracing can
therefore take many different forms but to the experienced gynaecologist,
who's seen a lot of tracks, a glance is all you need to know whether the situation is okay or not.
Decelerations may have uniform or variable morphology,

and be, in relation to the contraction, early and late.
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They're divided into:
1. Uniform decelerations
They have constant shape and can be:
 Early (previous or synchronous to contraction)

- duration from 20 to 90s,
- amplitude of 50 bpm,
- frequency drop of 200-30 bpm,
- frequencies above 100 bpm.
They are a consequence of fetal head compression and vagal activation (physiological conduction
during labor).
 Late (delayed with respect to contraction)

- at least 20s,
- amplitude of 40 bpm,
- frequency decrease of 10-20 bpm.
They are more dangerous than early ones because of reduced fetal oxygenation (the fetus "recovers
badly").
If you have a major deceleration, defined as a tank (extensive and long-lasting deepening), the fetus is in
distress and must therefore be pulled out. The greater the drop in bpm and the longer it lasts, the greater the
alarm for the fetus. The problem, therefore, is not the single deceleration (which may be due to the most varied
and contingent reasons), but the repetition of several decelerations and their long duration.
NB: late decelerations are universally considered a sign of fetal hypoxia.
2. Variable decelerations
They have a variable shape, are in variable relation
to the contraction and are determined by the
contraction of the ropeway. They are characterized
by a slight initial acceleration, followed by a
variable form deceleration (V, U, WW, S), finally
followed by a final acceleration.
According to the shape they are distinguished in:
 slight duration < 30s, frequency > 80 bpm,

 average duration 30-70s, frequency < 70bpm,
 severe duration > 60s, frequency < 70 bpm.
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The concept that decelerations contained in the frequency and limited to uterine contraction have no
particular pathological relevance is reiterated, while the "tubular" deceleration, with a considerable drop in
frequency and for a significant period of time, is a cause for concern.
The variable decelerations (variable precisely because they are not related to the uterine contractile activity)
are morphologically:
- more obvious,
- more irregular,
and are considered pathognomonic to umbilical cord obstruction. However, they do not always indicate real
danger to the fetus. In clinical practice, however, they always induce the doctor to decide to terminate the
pregnancy and extract the fetus, in order to avoid any harmful consequences for the child.
The concept is: even if there is reasonable doubt that the fetus may actually be in danger, in order to protect
itself and not to risk if problems are actually present, in the face of decelerations especially if relevant and
long lasting, the doctor always opts for the extraction of the fetus.
Finally, there are secondary characteristics of

variable decelerations that indicate prognostically
unfavourable factors, which therefore also indicate
immediate delivery:
 Decreased steepness of ascent,

 no deceleration oscillations,
 lack of initial acceleration,
 continuing compensatory tachycardia,
 lack of return to pre-existing basal rate,
 the appearance of decelerations doubled (one after

the other) and rounded.
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NB: cardiotocographic information must of course always be cross-referenced with all other pregnancy data
(mother's parameters, week of pregnancy, baby's weight, uterine contractions, etc.).
Fundamental difference between the two types of monitoring:
 BIOCHEMICAL precise ascertainment of the fetus' acid-base balance conditions, but with the limit
of giving precise but instantaneous information, therefore susceptible to change during labour
(which also lasts many hours),
 ELECTRONIC recording continues throughout the duration of labor, so it allows you to have
information about the entire course; limit is that it gives information of the type "all or nothing",
often inaccurate, if not even faulty.
Ideally, therefore, both types of monitoring should be used together, in order to get as much information as
possible. The limit to this is that the cardiotocographic trace needs staff to read it continuously and constantly,
which is very often not possible.
PARTOGRAM
It is a graph that describes the entire course of labour in childbirth (it should start from the moment of
diagnosis). It considers at the same time a series of components:
- degree of cervical dilatation,
- level of the fetal head relative to the birth canal,
- fetal heartbeat,
- maternal blood pressure and heart rate,
- color of the amniotic fluid.
In addition to the personal data, the type of labour and

obstetrical history, oxytocin and analgesics should be
indicated in the form.
In it it is then possible to relate in the same graphic
record:
1. degree of progressive cervical
dilatation,
2. level of the fetal head relative to the
birth canal.
It can be cross-referenced with biochemical or
electronic monitoring data and represents a very useful
means to retrace the stages of the entire duration of
labour (6h-10h-1g) in an accurate manner (also for the
purposes of medical-legal litigation, for example).
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PREMATURE BIRTH
The premature birth:
- affects 10% of pregnancies
- is one of the main causes of fetal death (70%); that is, fetuses that do not die because they have a
malformation, but only because they are born prematurely.
When we talk about fetal mortality due to premature birth, it corresponds to 70% of all fetal deaths in the
absence of malformations, we refer to a statistic that does not take into account the different services that
people in different geographical areas can access even within the same nation. In the event of a premature
birth, although not excessively, in an area where health services are few and poorly functioning, the baby
could die from a lack of ability to breathe, and in that case it would have been enough to use a catheter in the
nose to help the baby to breathe.
Premature birth, according to the WHO, is defined as the expulsion of the fetus and its appendages between 25
and 37 weeks (although in clinical practice premature foetuses, and therefore subject to resuscitation, are
considered to be fetuses even those born after 23 weeks). On the other hand, a fetus that is born before 180
days of gestation (25 weeks) is considered an abortion.
Consider that the pulmonary maturity is around 34 to 35 weeks, while the cerebral maturity is around 37
weeks. From this it follows that the foetuses most at risk of neonatal mortality and morbidity are those born at
less than 27 weeks, after which there is a progressive reduction in risk up to 35 weeks, beyond which the risk is
significantly reduced.
Likewise, premature fetuses under 1000g are more at risk of relics, while this decreases gradually as maturity
increases, especially over 1500g.
Premature parts are:
- spontaneous in 70% of cases (e.g. sudden rupture of the amniochorial membranes and irreversible
onset of labour)
- iatrogen in the remaining 30% (i.e. induced by the gynaecologist mainly to safeguard the health of
the mother, for example in case of gestosis, hypertension, preeclampsia, etc.).
Etiopathogenesis
The causes of premature birth are:
 deciduous and chorion-amniotic infections that cause membranes to rupture

 premature untimely rupture of amniochorial membranes (pPROM)
 maternal-fetal stress
 hypoxia uterus-placental
 haemorrhage
 pregnancy-induced hypertensive disorders not controlled by therapy
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 cervical incompetence
 diabetes mellitus (in this case, for example, pregnancy cannot be conducted at term due to excessive
fetal macrosomy).
 Chorion-amniotic infections, i.e. chorionamniositis, occur when the bacteria come into contact with
amnios via the ascending route following a cervical-vaginal infection (by far the most frequent) or
via blood (very rare).
 Vaginal infections that can give chorionamniositis are bacterial vaginosis and diseases due to other
infectious agents (including rarely viruses). Bacterial vaginosis is the most common infectious
vaginitis, it is due to a complex alteration of the vaginal flora in which the lactobacilli are reduced and
the anaerobes (Prevotella sp, Peptostreptococcus sp, Gardnerella vaginalis, Mobiluncus sp and
Mycoplasma hominis) grow in excess. Symptoms include grayish, thin, fishy-smelling, itchy vaginal
secretions. The diagnosis is confirmed by examination of vaginal secretions. If a vaginal swab is
found in a pregnant woman, it should be treated immediately with the right antibiotic so as not to risk
future complications (including preterm delivery).
In general in cervical-vaginal infections there is a local inflammatory response with release of
cytokines, bacterial products and degradation products: on the one hand, cytokines and bacterial
degradation products cause the activation of cyclo-oxygenases with consequent release of
prostaglandins, which cause uterine contractions*; on the other hand, bacterial degradation products
and macrophages such as proteases, for example, can cause the rupture of chorionic membranes**:
the two concomitant factors induce early delivery.
 As for maternal-fetal stress, the excess cortisol produced by the adrenals causes increased production
of prostaglandins that will directly stimulate the contraction of the myometrium. It should also be
noted that under fetal stress conditions (i.e. hypoxia), the fetus itself produces cortisol, which activates
the production of prostaglandins.
In the interval space, syncytiotrophoblasts release CRH, progesterone and estrogen in maternal and fetal
blood. Maternal cortisol passes through a maternal artery and enters the intermittent space, where it
stimulates the production of CRH by syncytiotrophoblasts. An umbilical vein in the fetus brings CRH into the
fetal circulation, stimulating the fetal pituitary gland to synthesize corticotropin (ACTH) and to stimulate the
synthesis of fetal adrenal cortisol and DHEAS. Cortisol and CRH stimulate the fetal lungs to produce the
protein A surfactant, which passes from amniotic fluid to amnios, where it stimulates the production of
cyclooxygenase 2 (COX-2) and the synthesis of prostaglandins E2. They pass through chorion and decidua to
stimulate the underlying myometrial cells to still synthesize COX-2 and prostaglandin F2α.
The professor explains an experiment in which he participated years ago in Australia; when it was not yet
known that cortisol was the fetal precursor of the beginning of labor. An experiment was carried out on a
pregnant sheep: a caesarean section was performed on this sheep, the head of the lamb was pulled out, to
which the pituitary gland was deconnected (entering through the nose), so that it could receive stimuli from
the cerebral cortex, but could no longer send endocrine signals to the rest of the body, so it could not even
cause the secretion of cortisol, which therefore the lamb no longer produced. At this point the lamb fetus was
reinserted into the uterus of the sheep that was sutured, and continued its pregnancy, but it never had the
stimulus to labor and then the lamb was then extracted with a further caesarean section. This experiment was
also carried out with rats and mice. From this we deduce that the absence of contractions can be caused by
problems of the mother, but also of the fetus.
 Uteroplacental hypoxia is caused by reduced uteroplacental perfusion; hypoxia on the one hand
causes IUGR (intrauterine growth retardation) and on the other hand locally causes the production of
uterotonic substances.
Risk factors
112X
Although 50% of cases occur in the absence of these, premature birth has risk factors that must be diligently
investigated in the course of a medical history.
We recognize: Socio-economic factors (in fact, while a person who is economically well often goes to get
checked, a person in a difficult economic situation typically neglects his or her health, does not get treatment
for infections at an early stage; the weight of socio-economic factors is all the more evident if we also consider
the crucial importance of prevention in gynaecology at all stages of a woman's life), local factors (such as
conization2, asymptomatic cervical dilation, cervical shortening, uterine malformations, uterine
fibromyomatosis, previous uterine surgery and abdominal trauma) and factors related to obstetric history
(such as nulliparity, a previous preterm delivery, two or more miscarriages, vaginal infections and recurrent
urinary tract infections).
Symptomatology and diagnosis
In the event of preterm birth or threat thereof you have in succession:
1. cervix modifications, with neck flattening associated with

cervical canal dilatation and centralisation. In order to
investigate these aspects, the internal uterine orifice
(OUI), the neck (when you visit a woman out of labor
entering with a finger into the vagina you can barely feel
the neck of the uterus posteriorly which is shaped like a
small cylinder, while when the woman begins labor the
cervix is centralized and touched immediately anteriorly,
also has a less clear shape with a hole in the center where
you can enter with one or two fingers more or less deeply)
and perform a transvaginal ultrasound that gives an idea of the length of the cervix and witness the
presence of funneling3;
2. descent of the presented part; Ultrasound with funneling
3. loss of mucous plug;
4. uterine contractions;
5. premature rupture of the membranes;
6. birth before the 37th week.
Other elements that may suggest a threat of preterm delivery, even if they are not symptoms of this, but more
than the prodromes are: fixed or intermittent menstrual cramps in the suprapubic region, fixed or intermittent
lumbosacral pain, abdominal cramps with or without diarrhea, more than one uterine contraction every 10
minutes painful or not and possible presence of risk factors.
With manual exploration the gynaecologist can already make a diagnosis.
Obstetrics and therapy
In case of risk of preterm birth, some procedures should be performed:
 Assessment whether risk factors or causal factors are present in the medical history
2
It consists of the removal of a truncated cone of the uterine neck which allows the tissue affected by the lesion to
be removed. It represents a risk factor for cervical incontinence.
3
Cervical dilatation begins at the OUI level, which widens and allows for invagination in the cervical canal of the
membranes and amniotic fluid. This modification is called funneling (less frequently wedging). In the absence of
dilatation the OUI is normally flat (T-aspect), in the presence of funneling it presents different aspects in relation to
the degree of cervical incompetence, initially Y-shaped, then progressing towards a V-shaped aspect in the
intermediate phase and U-shaped in the final phase.
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 Gynaecological examination with transvaginal ultrasound to assess the cervix

 Fetal well-being monitoring, performing an NST4 (i.e. a non-stress test) and flowmetry (via doppler)
 Monitoring of uterine contractility by performing a cardiotocography (actually a cardiotocograph is used
to do the NST which should give both information about the child's heart contractility and uterine
contractions).
 perform a vaginal swab for microorganisms, to see if there are any infections
 perform a vaginal swab for fibronectin, which is only present when the amniochorial membranes are
broken, so it gives information about a possible small rupture of the membranes that clinically would not
be clinically assessable due to the little fluid loss
 fetal pulmonary maturity is induced if 34 weeks have not yet been reached, using 12mg of beta
methasone every 12h twice, at least 24h before delivery. This induces at the fetal lung level *the
production of phospholipids and anti-oxidant enzymes, *the reabsorption of liquids from air space and
*the production of surfactant from type II pneumocytes.
 tocolytics are administered to prevent uterine contractions from causing childbirth. Tocolytics can be of 3
types, β2-sympathic mimetic agents (Ritodrine, which acts by reducing intracellular calcium levels), Ca-
antagonists (Nifedipida, Nicardipine; they act by inhibiting intracellular calcium flow) and oxytocin
antagonists (Atosiban, which blocks the entry of calcium into the cell).
As for the former, the most important side effects are maternal tachycardia with heart palpitations,
although there are others less frequent such as maternal vasodilation, pulmonary edema and fetal
tachycardia.
The second, the Ca-antagonists, have headache, flushing and asthenia as side effects.
Finally, Atosiban is a hospital-only and very effective drug with few side effects, which gives a blockage
of oxytocin receptors with few side effects, but which should be administered in continuous infusion.
(The cerclage (picture on the side), i.e. a surgical ligation of the

cervix to keep it closed, is an operation that is never carried out for
this purpose, at the limit in election when problems occur at 14-15
weeks of pregnancy. In fact, if the contractions are incoercible and
do not stop with any medication they can be much stronger than the
stitches, resulting in tearing of the uterus and massive bleeding).
Conclusions
The management of pregnant women at risk of giving birth early is a matter of cost-effectiveness, both in
terms of the woman's health and in terms of public health costs. Therefore, before making decisions, it is
necessary to evaluate: the gestational age, foetal conditions, maternal conditions and, if necessary, to
implement first a stimulation of fetal lung maturity and a therapy with tocolytics.
The most important aspect is perhaps the gestational era, because sometimes it can be very important to allow
a few more weeks of pregnancy using the already mentioned drug therapies, rather than extracting a child who
will perhaps die after a short time or remain with important sequelae, also very often leading to legal
consequences for doctors. In fact, even the use of a catheter to ensure breathing can cause the development of
serious infections, and the lungs themselves, which are not mature at birth, can lead to the development of
several diseases in more or less adult age.
4
The cardiotocography that is normally done today is called non-stress test, because it is not done in conjunction
with an administration of oxytocin, which leads to uterine contraction and therefore fetal hypoxia with a decrease in
uterine heart rate.
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pPROM
PROM is the untimely rupture of the membranes during labor (or just before, perhaps with the use of
aminorexi precisely to stimulate labor), while pPROM is the untimely rupture of the membranes that occurs
before 37 weeks. In fact, the rupture of the amniochorial membranes after 37 weeks is considered a
physiological traumatic event, while before 37 weeks we fall in preterm delivery.
Amniochorial membranes are formed by:

1) amnios, elastic layer, of cubic cells;
2) collagen, consisting of: compact layer, fibroblast layer, spongy layer, cellular layer, reticular layer. (It
decreases with gestational age);
3) chorion, consisting of basal membrane and trophoblast.
Collagen regulation depends on the interaction between metalloproteinases (MMPs) and metalloproteinase-
specific tissue inhibitors (TIMPs). An imbalance between MMPs and TIMPs causes the membranes to rupture.
The duration of pregnancy after PROM is inversely proportional to the week in which it takes place: if it takes
place at the end of the pregnancy in 80% of cases it will give birth on the same day, on the other hand if it
takes place before 26 weeks 40% of cases end after 1 week, although a small part of the cases may last even
more than a month; between 26 and 32 weeks the birth will probably take place within 1 week but in this case
the fetus has a much better chance of surviving.
The explanation for this phenomenon probably lies in the inability of the uterus to contract.
Diagnosis
The diagnosis of pPROM is made with the speculum by observing the exit of fluid from the external uterine
orifice and testing the vaginal presence of fibronectin, while an ultrasound scan shows the lack of fluid
(oligodramnios, anhydramnios).
Once pPROM has been diagnosed, it is not necessary to perform many vaginal examinations because there is
an increased risk of ascending polymicrobial bacterial contamination.
Instead, it is advisable to check the fetal well-being with a cardiotocograph (even if it is not effective before 26
weeks) and ultrasound, as well as assessing uterine contractions.
It is also good to check maternal well-being with a simple visit where you check blood pressure, heart rate,
body temperature and at the limit prescribe a PCR and blood count check.
Complications
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The main complication of pPROM is prematurity. Others are: bronchodisplasia, breathing difficulties,
ventricular bleeding, necrotizing enterocolitis, retinopathy, infections of the fetus and/or placenta,
anhydramnios, pulmonary hypoplasia and deformity.
Management
First of all, in the case of pPROM, antibiotic prophylaxis must be established, then it is good to induce
pulmonary maturity with the administration of cortisone; at this point a watch and wait approach can be
implemented and in the case of delivery if necessary.
Miatton Andrea 24-10-2019

Padoan Simone Gynaecology, Lesson
No. 8
Prof. Ambrosini
PLACENTA PREVIA, PLACENTA DETACHMENT, MEF, PUERPERIUM,

LACTATION
THIRD QUARTER METRORRHAGIA
One of the dangerous abnormalities in pregnancy is third trimester metrorrhagia. Most small blood loss during
pregnancy is nothing serious, but in some cases there is a risk of complications that can lead to the death of the
mother or fetus.
Basically there is a loss of blood from the external genitals. It occurs quite frequently, affects up to 5% of
pregnancies, and is a situation that requires attention.
Etiology:
A blood loss can be due to placental or extraplacental causes; if they are placental and are abundant, a
placental detachment or a placenta previa should be considered.
- Placental causes
o Untimely detachment of normally inserted placenta (22%): the placenta is normally inserted
but at a certain point, slowly, it detaches
o Placenta previa (31%)
o Breakage of previated jars (0.5%)
- Bleeding from extraplacentary causes
o Cervical polyps
o Cervical ectropion: an ectropion at the portio level could bleed during intercourse, so you
should always ask for this anamnestic data
o Rupture of cervical or vaginal vessels: this can happen during changes to the neck and body
of the uterus.
o Cervical cancer: the Professor claims not to have seen this phenomenon during pregnancy.
o Coagulation alterations: women who have particular defects of Leiden's HFR, factor II and
factor V elements
o Idiopathic
PLACENTA PREVIA
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The placenta previa is a placenta inserted abnormally a little too low and close to the internal uterine orifice; it
can even cover the internal uterine orifice. It can be classified in:
- Lateral (A): low placenta (isthmic), but more than 3 cm from the OUI; it can give some small
bleeding, rarely problems either in spontaneous delivery or in caesarean section.
- Marginal (B): less than 3 cm from the OUI; very low placenta, near or in front of the isthmus but not
above the OUI
In theory, the baby can also be born from spontaneous birth, but if a caesarean section is necessary, it is
necessary to know if the marginal placenta is attached anteriorly: in such a case, it is located in the area where
the surgical cut is normally made and this makes the operation difficult; in the case of a posterior marginal
placenta there are no problems.
- Central: the placenta covers the OUI: the patient will certainly not be able to give birth spontaneously
by vaginal means.
o Partial (C): if the placenta only covers a part of the OUI
o Total (D)
Frequency [from slides]:

- Primipare 0.26%
- Multipare 0.56%
- Total 0.4%
According to the Professor, in
Padua obstetrics clinic the
frequency is higher, being a
third level center.
Predisposing factors
- Multiparity: it is assumed to be linked to the fact that the placenta had previously created small scars
on which the embryo then attached itself and grew.
- Advanced maternal age
- Pregressa placenta previa
- Pregresso cesarean cut: always because the embryo can attach itself in the area where the cut has
created a solution continuously
- Uterine fibroids/anomalies anatomy
- Pregresse endometritis
- Multiple pregnancy
- Smoking: Prof says he doesn't know why smoking is predisposing and reiterates that smoking is
always one of the risk factors.
The placenta previa can be either primitive or secondary:

- Primitiva
o Embryo nesting at istmic level
- Secondary
o Normal nesting
o Poor uterine vascularization
o Excessive placental development
o Diffuse placenta
This type of placenta usually also has bad vascularization, so it is placentas that come off more easily. The
detachment is due both to the bad insertion and to the fact that the more caudal position in which it is located
suffers more dilatation and relaxation. It's like a piece of scotch: you can stick a piece of scotch on one hand,
but as soon as the hand starts to open or close, the scotch immediately comes off.
Mechanism
- Placental insertion at the istmic level
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- Lower uterine segment distension

- OUI dilation
- Placental fabric: Placental fabric is not so stretchy, so it tends to come off.
- Placental detachment: Normally you don't detach the whole placenta, but you detach small pieces that
then stick together again.
- Bleeding: consequence of the detachment of the placenta pieces
- Inability of the myometrial fibers of the SUI to contract adequately to make hemostasis : this is
because the area of the isthmus has the ability to stretch but not to close, unlike the areas of the bottom
and the body that are characterized by a very strong musculature, which tends to make mechanical
hemostasis through contractions and contractures, closing with a fist.
The placenta previa is easily diagnosed because you only need to do an ultrasound to see its position. If a
placenta previa is discovered, it is to be hoped that it will not cause problems, but if there are problems it is
still problems that arise in the third trimester, which is less serious than having earlier complications.
Symptomatology
It consists of the presence of bleeding in the third quarter.
- Painless! the pregnant patient feels nothing, and at some point notes the blood loss
- Bright red
- Earlier in power plants (28-34 weeks)
- Marginal and Lateral after 34 weeks
- Spontaneously but recurrently ceases: they are patients who often go to the emergency room
The event of the placenta previa is not an acute event in which the placenta detaches entirely; it creates anxiety
because there is bleeding but it can be managed, and usually with rest everything is settled. It is important to
distinguish this phenomenon from the normally inserted placenta detachment, which is a very dangerous event
in which timely intervention is required.
Differential diagnosis
There are various causes of bleeding, but in the third trimester the placenta detachment and the placenta previa
are the main ones.
- Placental detachment
o Pain: You have a brief moment of pain, knife-stroke type, which lasts for a short time.
o Dark red: the pain follows; when a piece of placenta previa is detached, there is almost
always bleeding because the part that detaches is the lower portion near the isthmus, then the
blood immediately falls down into the neck and then into the vagina. In the normally inserted
placenta detachment, on the other hand, you could have a detachment that starts from the
upper portion and continues downwards, and consequently you could create a blood
collection that does not go down into the vagina and therefore does not make the bleeding
itself manifest.
In case of pain with a knife, even without blood, you always have to check.
o Uterine contracture
- Rupture of cervical or vaginal vessels: there are some very important vessels in the cervix, so when
there is distension of the neck it is normal that some vessels may rupture causing a small hemorrhage.
o Venous Blood
o Trauma
Evolution
- Recurrent bleeding, patients often come to the emergency room several times.
- Gravescent hemorrhages
- Anemonization: if the small bleedings are continuous, or if they are important
Maternal complications
- Anemia
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- Intra-post partum haemorrhage

- Hysterectomy: it only comes to this under special conditions
- Transfusions
- Mortality 0.03%: the Professor claims that he has never seen anyone die from placenta previa, but
says that Padua is still a third level structure.
Fetal complications
- Progressive reduction of exchange area between mother and child
- Maternal anemia
- Fetal blood loss
- Abnormal presentation due to altered uterine geometry: "technically no" [verbatim NdS].
- Preterm delivery: if the patient has a placenta previa, she will not normally complete it
What you do:

- Speculum: you insert a speculum into the vagina and look to see if the blood comes out of the porthole
or somewhere else; if the patient complains of leaks, you should always check that they do not come
from the urethra, vulva, vagina, neck, etc., before thinking about placenta previa or untimely
detachment.
- Ultrasound scanning
- (vaginal examination)
Therapy
Gestational age/bleeding age: the most appropriate assessment and decision must be made from time to time.
- Fetal maturity: elective caesarean section, pulling out the baby is the first choice but it is always age
and dependent child; if you have a dangerous situation and gestational age allows it, the best choice
is always to pull out the child
- Maternal or fetal impairment (severe haemorrhage): urgent caesarean section
- Prematurity, stable conditions: conservative management
Complications
- Secondary abnormalities: sometimes these placentas insert badly
- Poor lower uterine segment decidualization
- Difficult seconding: due to abnormalities in seconding and poor decidualization, the placenta remains
attached
- Few muscle fibres
- Difficult hemostasis from the muscular globe; beyond the normal phenomena of coagulation and the
drugs that can be administered, the fact remains that in that area of the uterus there is a lack of the
ability to contract (a phenomenon called the safety globe, in which the uterus closes with a puncture to
make mechanical hemostasis).
- In 7-10% of cases of placenta previa, the placenta is also accreted: the villi of the placenta have
inserted too deep into the tissue (they do not only reach the basal tissue). As a result, the placenta
cannot be detached but must be torn and in doing so the tissue is torn ("and it is a disaster").
- Anomalous adhesion of the placenta to the uterine
wall (basal decidua is missing); they may occur:
o Placenta accreta: chorionic villi directly
adhering to the myometrium
o Placenta increta: chorionic villi deeply
invade the myometrium.
o Percrete placenta: the chorionic villi
perforate the uterine wall (myometrium and
serum) and reach the adjacent organs.
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The Prof claims to have never seen a percrete placenta, just a few uncreeps and a lot of accretions. Sometimes
you have to tear the tissue and then rebuild it, but it's not always that easy, so there are cases where you have to
remove the uterine organ.
- Incidence increasing: 1 in 2500 pregnancies
- Risk factors:
o Advanced maternal age
o Multiparity
o Caesarean sectioning: it is certainly an important risk factor
o Pregressa uterine surgery (RCU)
o Placenta previa! important risk factor
o Previous placenta previa
o Anterior placenta on the surgical scar from the previous C-section!
- Midwife emergency!
o Severe bleeding: also affecting patients already anemic
o Womb rupture
o Transfusions
o Hysterectomy
o Reconstruction of neighboring organs: if the placenta has invaded the adjacent organs
o Maternal Mortality: It may happen that you pull out a baby who is fine but the mother dies
from it.
- Diagnosis:
o Anamnesis: risk factors, it is always done
o Instrumental: ultrasound and MRI
o Clinical: difficult placental detachment when pulling out the placenta
o Histological
PRIOR TANKS
- Umbilical cord vessels covering the OUI
- very rare (1:5200 pregnancies): the Prof has never seen one
- associated with a veiled or marginal insertion of the cableway
- fetal mortality 95%!
UNTIMELY PLACENTAL ABRUPTION

Detachment of a placenta normally inserted from its seat before delivery. Cause bleeding!
The following cases may arise:
- the mother arrives in the emergency room already with the dead fetus.
- the fetus dies during cesarean section
- the fetus is unwell despite the Caesarean section.
- the mother can go into hemorrhagic shock, and sometimes you can't save the mother.
The problem is that the detachment happens very quickly; there is the pain at the knife stroke, but it tends to
decrease, and if there is no bleeding, the woman is inclined to wait to see how the situation evolves.
Maybe:
- external 70%: the blood from the detachment area creeps between the membranes and the
myometrium
- 30% occult: blood remains retained between placenta and uterus
Features:
- Total or partial: will start from partial and become total (because it does not detach all at once)
- Incidence: 1 in 200 pregnancies
- Responsible for 10% of perinatal mortality
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- Applicant! If a patient has had an untimely detachment, in the second pregnancy you have to think
about untimely detachment.
COMMENTS AND GENERAL CONSIDERATIONS

[in the next part the Professor answers some questions and makes some personal comments, without following
the slides for explanation].
Question: I saw an MEF in pathology at 37 weeks. Since the woman had had an abortion before, couldn't she
be delivered earlier?
Answer: In the meantime this woman had had an abortion in the first trimester, so an absolutely physiological
thing in pregnancy. If a patient has only one abortion, it is not part of poliabortivity and therefore not one of
the patients that should be studied to find the cause of the abortion.
The guidelines require us to give birth to patients no later than 42 weeks; there is a lack of personnel, so we
cannot give birth to all women at 39-40 weeks. It is true that if you induced the birth at 39 weeks to all women
you would probably reduce the MEFs (which occur without warning), but imagine: if women giving birth at 41
weeks + 3 would be sent to the emergency room at 40 weeks when they are still without contractions, we
would be full of improper hospitalizations in the obstetrics clinic, we would have to stimulate all these women,
some of them would not respond to the stimulation so they would be directed to the cesarean section, we
would stuff ourselves with people who a week later would have a regular labor and we would do a bunch of c-
sections to women who would not need them. In large numbers, the current system is better. On the other hand,
those who do not have any kind of initiation of labour within 41 weeks and 5 days must be induced and must
be given birth one way or the other; it is obvious that in that time interval some MEF escapes us.
Question: he was 37 years old, wasn't that young, wasn't it better to schedule a C-section, or an induction?
Answer: The indication for caesarean section is not 37 years of age or abortion, otherwise everyone should
have a caesarean section. The age of 37 is not a danger zone, on the contrary it is now a zone of normality
(beyond the non-EU population).
When you see stars who have children at 50 in the newspapers, it's always about egg donations. It is a
heterologous type of fertilization in which the eggs of another woman are used. This is the solution to the
problems of those who are unable to have children with technology, those who do not have eggs, those who are
in menopause, those who have lost their ovaries, etc..
Question: is it legal in Italy?

Answer: yes, it has been legal for a few years. But, personally, if I had to give my sister an egg donation, I
wouldn't let her do it in Italy. I personally deal with egg donation, both in Italy and abroad. Today in Italy
donors have to decide to donate eggs without any incentive: the donor should pay for all genetic, infectious,
etc. tests to verify that she complies; then she should do all the drugs; then she should go to the operating
room. Abroad, on the other hand, the donors are paid (about 1500 euros) and the examinations are done by the
facility, which is still a complete checkup.
Usually the egg donation centres are the university headquarters; Padua could be a good place because there
are a lot of young students who would create a good influx.
In Italy what you do is to choose a donor who is phenotypically as similar as possible to the future mother, but
without knowing who she is; in America, however, you can choose the donor by seeing how much she has
taken at maturity and graduation, what physical she has, how much physical activity she does, etc..
In Italy 6 eggs cost 3400 euros, but they are frozen eggs that are then thawed and then fertilized, so they lose
quality (the egg cell is a large cell with a lot of cytoplasm and the freezing and thawing phase makes it lose
quality); In some states, instead, it is possible to have a personal donor, therefore, if the donor produces 15
eggs, all the eggs would be fertilized, all the blastocyst would be generated and then two blastocyst would be
implanted and the others would be frozen (in this way the chances of pregnancy are enormous).
In Italy the uterus for rent cannot be done, and this is a question that arises in cases of particular problems and
for male homosexual couples.
Question: Ethically, what is the difference between renting out your uterus and giving up your eggs?
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Answer: I don't deal in ethics. Everyone has their own ethics, but in Italy, the law means that their personal
ethics have no relevance. As far as the law allows, it is done, and our politicians have decided that in Italy you
cannot make the uterus for rent. Law 40 of 2004 was an extremely restrictive law and until 2009 it made work
very difficult; today there is a more permissive law.
The professor then says his opinion on the referendum on assisted reproduction, arguing that the majority of
the population is not interested in the problem simply because it does not concern them directly.
Question: you said that in Italy 6 eggs cost 3400 euros, the money goes to the structure to cover the expenses?
Answer: in reality the procedure can be done in private centres and in public centres, and in public centres
health care provides a reimbursement; in Veneto there are still some problems to start this procedure, but for
example the Friuli region already implements it.
It has to be said that 99% of heterologous fertilizations are done in private, because a segment of the
population (between 35-65 years old) that has some money to invest in this area is interested.
Italy, however, is a very fortunate country, because, even if with different timescales from the private one and
with less equipped laboratories, you have excellent public centers where you pay according to income,
sometimes even having free access to the procedure (including medicines and visits). Sometimes there are
excesses, the funds for which could be invested elsewhere: in Veneto the procedure can be free up to 50 years
of age, although the success rate over 47 years of age is 0% (only medicines are paid out from 1500 to 2000€).
Between 30 and 40 years of age, success is 50%.
[end of speech part]
Untimely detachment of the placenta

It is recurrent, tending to recur in subsequent pregnancies.
Mechanism:
- Bleeding in the basal decidua
- Hematoma separating placenta from myometrium
- Loss of placental function
- Reflex contracture of the uterus
- The retroplacental detachment area increases
rapidly to the edge of the placenta.
o Occult haemorrhage (retained inside the
uterus): only causes pain to the mother,
which may not present itself to the doctor.
o External bleeding: the blood drains the membranes from the deciduous and appears on the
outside. It alarms the mother who shows up at the E.R., allowing the woman and possibly the
baby to be saved.
Risk factors:
- advanced motherhood
- black race
- gestational hypertension, preeclampsia,
- multiparity
- twin pregnancy
- polydramnios
- smoke/cocaine
- previous pregnancy complicated by separation (recurrence 1:8!)
- PROM
- Traumas
The diagnosis should be made with the clinic, suspecting any dark red haemorrhage in the third trimester, even
if small, not correlating in any way with severity. The suspect must also be present for continuous uterine
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hypertonic pain. The ultrasound, which shows a retrochorial hematoma, and the cardiotocographic trace,
altered by fetal suffering, can also help.
The complications are divided into fetal and maternal, the latter are hypovolemic shock, post-partum
haemorrhage and uteroplacental apoplexy, the former substantially coincide with perinatal death (15-65% of
untimely detachments).
The mild forms may provide a conservative approach with control of vital parameters, while the severe forms
oblige to carry out the delivery quickly, even by caesarean section.
FETAL ENDOUTERINE DEATH

Death occurred after 180 days of pregnancy, when it is assumed that you can have an autonomous life (at 23
weeks survival is 20-30%, at 25 of 50%). It's very much related to motherhood:
19/1000 if maternal age <15 years;
8/1000 with 20<E<34
22/1000 with E>40.
Unfortunately, it is not always known why the fetus died, even after examination of the mother and the fetus
(pathological anatomy). Of course it is important to perform tests on parents looking for situations that may put
at risk subsequent pregnancies, such as chromosomopathies, coagulopathies or the presence of maternal
autoantibodies (antiphospholipids, anticardiolipin) and SLE.
You can distinguish MEFs:

to intact membranes, frequent macerative episodes,
or incomplete membranes, more exposed to external infections with putrefactive episodes.
Twin pregnancy
It is difficult to treat a twin pregnancy in which one of the fetuses dies; it is hoped that the dead fetus will
dehydrate without maceration or putrefaction, but if this is not the case it would be necessary to cause the
delivery of the other fetus as soon as possible. In 50% of cases, pregnancy can continue without intervention.
In most cases the mother does not notice anything and the MEF is detected on ultrasound by the following
signs:
- Absence of cardiac activity
- Spalding (skull bone overlapping)
- Tissue oedema (mainly skull cap)
- Spinal column kyphosis-scoliosis: very important sign even if difficult to assess; usually you see
children immobile and rolled up on themselves. The professor cites, for example, an ultrasound
performed on a mother of 124 kg and in twin pregnancy, in which, in addition to the fat, the
mechanical waves had to cross one of the two fetuses before reaching the other, with consequent loss
of definition.
Premonitory signs
- Marked reduction in fetal movements
- Marked growth defect
- Non Stress Test with no variability
- Altered fetal flowmetry
- Cerebral vasodilation
- ARED at umbilical artery level
- Umbilical vein with presence of pulsation
The best treatment in case these premonitory signs are detected is obviously the completion of childbirth by
amniorex, oxytocin or prostaglandins.
The following events may develop: bacterial infection or disseminated intravascular coagulation, following the
release of fetal necrosis factors, in particular thromboplastin substances.
PUERPERIO
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Puerperium is the period of time between the completion of childbirth and the return to normal of the female
genital organs; it begins as soon as the baby is born, even before the fetal annexes leave.
After the birth you stay another two hours in the delivery room, where you manage the exit of the fetal annexes
and check your heart rate, blood loss and urination. Once you have made sure that everything is normal you
can go into puerperium, an area of the gynaecology department.
Usually ovarian activity is resumed within 6 months, but in most women the first menstruation is within 6-8
weeks, or slightly slower if breastfeeding, as high levels of prolactin can interfere with the hypothalamic-
pituitary-gonadal axis. Sometimes menstrual irregularities and anovulatory cycles can occur. Milk production
depends on prolactin, and ends quickly if it is blocked with, for example, dopamine.
Uterus
Gynaecologist's duties in puerperium:
- assess how far down the uterus goes, using
the navel line as the 0 line. In particular,
there is a decrease in myometrial cell
volume and autolysis of stromal or
parenchymal proteins. A uterus that doesn't
drop is a dangerous uterus.
- uterine palpation to feel its consistency
(initially it is hard and is called a safety
globe).
- evaluation of the lochi, serum-serum
secretions normal in the first days after
childbirth and which may persist for up to 3-
5 weeks. At first they are abundant and
haematic, then increasingly scarce and
whitish.
A normal uterus is 6-7 cm long, while in the first hours after delivery the neck alone is 5cm long. In
puerperium a woman has uterine bites, pains, sometimes irradiated to the iliac pits, given by the contractions of
the uterus that is returning to its original size. They're stronger in multiples, and associated with larger
lochiations. They increase during lactation because the increased production of oxytocin stimulates
contraction.
Question: How do I know when I could ovulate again and have a new pregnancy?
Answer: you can't know, you have to wait for the foreman, the first menstrual cycle after pregnancy.
There is a regression of adaptations made during pregnancy:

- The organs regain their basic anatomy, e.g. the stomach is no longer forced against the diaphragm and
the lungs can expand freely as normal breathing resumes.
- Predominance of the vagal system, with bradycardia and hypotension, as well as drowsiness and
asthenia.
- You may have an emotional lability, with the possibility of transient puerperal depressive syndrome,
characterized by ease at crying, depressive crises, excessive concern for the newborn, or not wanting
to recognize it. When you notice these symptoms, you must immediately inform the psychologist and
your superior, to prevent suicide (10 cases per year in Italy, completely avoidable). Emotional
instability can occur both in the first few days after the birth and in the following weeks, so it is
advisable to make later appointments in hospital or with your gynaecologist.
- After seconding the cardiac output increases by 30%, with small episodes of hypertension, usually
self-resolving in a few weeks. After just one week, you're back to pregravity plasma volume.
- Progressive disappearance of varicose veins, which are accentuated in pregnant women due to the
obstructed venous return from the lower limbs.
- Resolution constipation and meteorism, especially the latter very present in the pregnant woman.
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- Resolution hemorrhoids, present in the pregnant woman due to the difficulty of venous return.
- Most pregnant women will have difficulty containing urine up to 6 months to 1 year after delivery.
- End of fetoplacental activity.
- Beginning galactopoiesis.
- Recovery of sex hormones secondary to ovarian activity.
Prolactin increases progressively during pregnancy due to the action of estrogen and placental progesterone,
which inhibit dopamine secretion.
1st quarter 25-60 ng/ml
2nd quarter 50-120 ng/ml
3rd quarter 90-250 ng/ml
4-5 days post partum 50 ng/ml, but with significant increase during and shortly after sucking . If you don't have
sucking, the levels drop to normal levels in a few days and the breast no longer produces milk.
MILKING
Nursing is not as pleasant as it sounds. At first it is very painful, because the baby is voracious and tends to
form rhagades on the nipple, so the teacher suggests to soften it a few months earlier with almond milk.
During the first 4 or 5 days of puerperium there is no milk, but a small amount (50-200ml) of colostrum, a very
viscous and yellowish liquid, full of proteins, immunoglobulins and fat, useful to fatten the baby who has lost
weight because he has not fed for a few days.
Preparation of the udder begins during pregnancy, under the action of estrogen and progesterone, which at the
same time inhibit the production of milk through the mediation of dopamine. There is development not only of
adipose and connective tissue, but especially of glandular tissue.
If you take dopamine, lactation stops in a couple of days.
There may be extemporaneous emission of fluid during pregnancy, which should always be assessed by a
gynaecologist. Milky whipped is distinguished by:
- Increased congestion and turgidity of the udder.
- Increased local temperature.
- 5-10 days: milk with an intermediate character between colostrum and final milk
- 10-15 days: mature, white milk with both IgM and IgA, as well as fat and lactose.
- Fall in estrogen and progesterone and decrease in dopamine levels, followed by removal of peripheral
blockade of prolactin receptors.
- Lactogenic hormones: ACTH, GH, Cortisol, TSH, T4, Insulin.
- Presence of the mammile-hypothalamic-pituitary reflex, an excitatory reflex that allows the
maintenance of milk secretion. Some women can breast-feed up to 2 years old.
- Between the 3rd and 4th month the production is maximum and almost a liter per day.
There is first an accumulation in the galactophor ducts (pre-milk; low content of proteins and lipids), then
sucking stimulates the secretion of oxytocin, with contraction of the muscle cells of the excretory ducts.
Oxytocin can also reach the uterus, so some women experience contractions during breastfeeding. This
promotes the involution of the uterus.
Advantages
- Non-allergenic nutrition
- Sterile and at suitable temperature
- Facilitates the creation of the baby's intestinal flora
- Improves the bond between mother and child
- Favoring the involution of the uterus
In the first few days you have 6-8 feeds. In the event of insufficient emptying, manual emptying must be
carried out to avoid a breast engorgement, which can result in mastitis. In the case of mastitis, the baby cannot
feed from the inflamed breast.
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Halfalira Laura 31-10-2019

Righetto Silvia Gynaecology, lesson 9
Prof. Ambrosini
PROTRACTION OF PREGNANCY, OPERATING BIRTHS, FETAL WELL-

BEING, AMENORRHOEA
PROTRACTED PREGNANCY
Prolonged pregnancy is defined as any pregnancy lasting more than 42 full weeks (294 days) counting from
the first day of the last regular menstruation. It has an
incidence of 3-12%, so it's not that rare.
Looking at this chart, we see perinatal mortality in

protracted pregnancy.
In the years 1943-52 it was very high, then in the years
1977-78 closer to us, but still 40 years ago, it was very
low.
What are the consequences for the fetus with a protracted

pregnancy?
 An increased chance of perinatal mortality, so if you keep him in your belly either way there's a better
chance he could die;
 fetal macrosomy, in fact, fetuses reaching 42 weeks usually weigh close to 4.5 kg;
 shoulder dystocia: in spontaneous childbirth it increases by about 18%, a lot;
 aspiration of meconium, the fetus often during childbirth due to defecatory stress and then aspirates
and swallows the amniotic fluid together with these pseudofaeces;
 the oligoidramnios, the placenta is sometimes no longer able to do that resorption and production of
amniotic fluid and therefore the baby has little fluid;
 the suffering of labor.
What are the consequences for the mother? Obviously a traumatic birth.
Nowadays we induce labor at 41+3 s.g, some structures do it at 41+5, but beyond this
term you can't go, you can run into medical-legal problems. The C-section is
obviously done if we have no other alternative and we have to take the baby out.
OPERATING PARTS
By operative parts we mean those real obstetrical operations, one of these is the
external turning, that is when we find a breech fetus, with the podice that presents
itself on the upper excavation and then we turn it so that we have a normal vertex
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presentation; it must be performed within 37-38 weeks, before it makes no sense, afterwards it becomes too
difficult and the chances that the uterus can be broken is very high.
Another manual operation that can be done at the beginning of labor is to correct the head that is very or very
little deflected (right image), i.e. when the presentation is not apex but is unfavorable (syncline, forehead or
face).
So what's it gonna take? Surely a good obstetrician who has understood that the presentation is wrong, and of
course a good gynecologist who knows that it is possible to reposition it and knows how to do it.
These manual operations include attempts to manually correct certain mechanical dystociae, such as failure of
internal rotation or sacral rotation of the occiput. When the child essentially does not come down because
he cannot do the internal rotation, you have to help him to do it, or when you have a sacral rotation of occiput
and then you have to turn him completely. These are delicate manoeuvres, because the child's head has bones
that have not yet been welded and therefore allows you to reduce the diameters a little bit, but it is also true
that performing abrupt manoeuvres can cause damage. For many years, "operational birth" meant above all the
application of forceps, it is a tool that can be with parallel branches or overlapping branches, it always has
two, you insert one at a time and then reconnect them with their fulcrum.
Naegele Forceps on the left;
Kielland forceps, right, more

particular because it has
overlapping branches, no pelvic
curvature, narrow and elongated
spoons and "lateral ginglimo"
articulation.
It is an ingenious tool for the fact that it not only allows us to take, rotate and pull but
also allows us to place it in such a small cavity, as you insert one branch at a time.
So we can not only pull the baby, but we can also move him, turn him around and let
him out on his own, because if he hasn't managed to do the internal rotation, we help
him. For example, in the case of the sacral presentation of occiput, he can't get down,
we can try to make his head spin completely. However, you have to be very careful because they are all
activities that need a lot of experience, because otherwise you can also do harm to the child.
Until 35 years ago the use of forceps was wild, it lacked the medical forensic danger we face today.
If we see today people aged 35 years and over with a skull a bit wrapped up, not perfectly round, or with a
draft, without a doubt are the results of forceps damage, small fractures caused by the instrument. It could
happen either because he was wrong to put the branches, which
must always be parallel, or also because too much force or
pressure was put on them.
Burton's forceps, another particular instrument, is no longer used

today because if I have patients with a rachitic pelvis, the
cesarean section is performed without thinking twice, but years
ago in those flat, rachitic pelvis, this instrument was used when
the child was in the middle excavation; thanks to the mobile
branch it allowed to enter, turn and find a solution even in the
most difficult cases.
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When you pull a child, the maneuver must not be static, but dynamic in the sense that you have to use the
arms, legs, force, so a good operator does not just pull but bends, uses the legs, bends the back, must feel when
the child turning it and turning it has found the right space and axis to pass and must use the whole body,
dynamically.
Another forceps is that of Pestalozza: it has an absence of pelvic curvature, it has parallel branches, small and
transversal handles, elongated and narrow spoons and it is reserved only for low perineal plane applications, so
it is a forceps that has great strength, and it is applied when the head is in the lower excavation; you can use it
also during Cesarean cut.
The conditions allowing the application of forceps are:

 complete dilatation, you can never use it if there is no dilatation, because the baby won't come out;
 absence of fetal-pelvic disproportion, are calculated with ultrasound, hands, and experience;
 fetal head deeply involved in the inferior pelvic excavation;
 broken chorio-amniotic membranes;
 fetus alive, because if it were macerated, it could, of course, unfortunately rupture.
Summing up the actions of the forceps are: rotating, reducing, and pulling.
Once you have pulled your head and disengaged, found the right diameter, the instrument is disarticulated and
normal childbirth assistance continues. You release from the fulcrum, pull out one branch and then the other
and then the birth takes place in a normal way.
Traction must be exercised with both arms of the operator and must be on the axis, in an active manner, to
adapt the transit of the fetal head to the different morphology of the birth canal.
These are images of trauma to the fetal head. The image above on the right shows two cephaloematomas, a
sub-periosteal blood collection, which, unlike birth cancer, is bordered by one or more cranial bones. It is a
haemorrhage that does not cause damage to the child; sometimes, especially in premature babies, the trauma
can affect the cranial bones themselves with very serious consequences in this case on the underlying brain
structures.
The Vaccum or Obstetrical Suction Cup has only a pulling action and a
reduced rotating action, it must be put at full expansion or at least 6 cm, it
needs less space than the forceps, because we only have to create the vacuum,
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to have the possibility to pull the fetus outside. A metal cup of various sizes is used, and it is much easier to
apply it to the fetal scalp than the forceps themselves. Obviously, an incorrect application of this method on the
large fontanelle can cause very serious injuries to the underlying brain structures. The cup should be put a little
bit of bias and then placed with the help of both hands, so as to put it on the scalp and not pinch portions of
uterus and vagina.
CAESAREAN SECTIONING TIME
Prof. skips slides 41-48 as already explained.

The overwhelming majority of Cesarean cuts are currently performed by fetal indication or interest to adhere
to the inspiring principle of Modern Obstetrics to give birth to "the best possible baby" in every pregnancy.
Nowadays it has become a dogma that if you perform a C-section on the first child, you don't have to do it on
the second. What they used to say years ago, that is, first caesarean section and then always caesarean section,
today is no longer respected, if it is possible to give birth spontaneously, it can be carried out quietly.
Unfortunately, there are cases in which it is necessary to remove the

uterine organ, due to an ongoing bleeding that no longer allows us to
wait, because the uterus is no longer able to contract, to make the
globe of safety and therefore we must remove it to save the life of the
patient. It is therefore necessary to connect the uterine vessels, which
are lateral to the uterus, it is also necessary to detach it from its
ligaments: the round ones, the posterior uterosacral ones, anteriorly
disconnect the bladder, close the lateral vessels including the uterine
artery. On the left is an image of a removed pregnant uterus.
Where we leave only the neck, to get support, but we remove the
uterine body completely and close the vessels.
ASSESSMENT OF FETAL WELL-BEING
One important thing to say is that the journey of 15-20 cm that the fetus has to make when it has to pass
through the upper, middle and lower excavation is the most dangerous journey it will make in the first 40 years
of its autonomous life. We do not know why 40 years, but in any case this is a phrase that means that it is
extremely dangerous this journey that the fetus makes to get out into the outside world. Consequently, a
Caesarean section greatly reduces the risk of complications. The danger of this trip is largely attributable to the
effect of uterine contractions on fetal intrauterine oxygenation, this effect in turn changes depending on the
degree of functionality of the placenta existing at the beginning of labor.
If the placenta is normally functioning and if uterine contractions maintain normal characteristics in rhythm,
intensity and duration the effects on fetal intrauterine oxygenation will be the result of the balance between:
- factors that tend to improve fetal oxygenation;
- factors that tend to worsen fetal oxygenation.
For this there is the gynaecologist, the midwife, the cardiotocography, the measurement of metabolic acidosis.
The factors that tend to improve fetal oxygenation during uterine contraction are:
- the slowing down of circulation in blood gaps will allow for a progressive increase in trade;
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- the longer time usable by the exchanges will make it easier for O2 to pass from mother to fetus thanks
to the "double Bohr effect";
- At each uterine contraction the fetus benefits from a kind of autotransfusion of oxygenated blood,
since the blood contained in the villi is "squeezed" towards the umbilical vein and then towards the
fetal heart;
- the contraction of the myometrium during the contraction facilitates the venous return to the maternal
circulation, increasing the venous pressure in the uterine veins, and thus indirectly improves the
possibility of conveying oxygen to the fetus. So the contraction itself is positive.
The contraction of the myometrium will first occlude the uterine veins causing a slowing of the circulation in
the blood gaps, then, acting also on the arterioles, it will reduce the uterus-placental blood flow.
Transplacental respiratory exchanges exploit the so-called "avalanche effect": i.e. you lower saturation and
always send oxygenated blood, this obviously if the placenta works well, if the funiculus works well and
therefore you have two arteries and a vein, it does not work as well in those fetuses with only one artery.
The contractions of the myometrium causing an increase in

endouterine pressure squeeze the fetal blood from the
chorionic villi to the umbilical vein and then to the fetal heart,
working almost like an additional heart pump, at the same
time the blood from the uterine veins will be pushed to the
maternal heart.
The blood reaches the fetus through regular vessels, then

imagine what happens when you go back: from the picture
beside you can see that the vessels are getting smaller and
smaller, becoming microscopic, in the chorionic villi, in the
gaps where the blood is deposited at low circulation and
therefore deoxygenated.
The factors that tend to worsen fetal oxygenation during uterine contraction are:
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- reduction of uterus-placental blood flow;

- increased intramniotic pressure > increased fetal peripheral resistance due to a poorly functioning
placenta > fetal hypertension because the fetus' heart pumps more > on the carotid baroreceptors >
fetal bradycardia evaluated by the cardiotocograph > reduction in fetal blood volume/minute;
- increased pressure on "fetal triggers" > vagal reflex > fetal bradycardia > reduced fetal
volume/minute;
- supine hypotensive syndrome;
- Poseiro effect: consists of a uterine contraction that causes a change in uterine position and
compression of the maternal abdominal aorta. This phenomenon manifests itself during a uterine
contraction with the disappearance, in 30% of cases, of one or both femoral wrists and a consequent
reduction in blood supply for a period of time longer than that caused by the uterine contraction.
What the prof has noticed is that every time there is a contraction of the venous return of the vena
cava on the right side, you will easily have a hypoxia problem and therefore a theoretical fetal
hypertension, with bradycardia and consequent fetal hypo-oxygenation.
If the placenta is normal functioning and uterine contractions are normal in rhythm, duration and intensity, the
balance between factors that improve and factors that worsen fetal intrauterine oxygenation is positive, so
much so that fetal blood pH values are higher during the acme of contraction than during the pause, and
therefore most fetuses are fine.
It's different when the contractions are there but the fetus can't go on, or the placenta doesn't work properly
anymore, or the compensatory effects aren't there anymore.
Under physiological conditions, fetal oxygenation worsens only towards the end of the expulsion period when
uterine contractions become more intense, longer and closer, for this reason there is a slight respiratory
acidosis (>pCO2) which results in modest fetal cyanosis but also in stimulation of the bulbar centers for the
initiation of spontaneous respiration. So it is normal at a certain time to have a fetal hypo-oxygenation, so there
will be only at that moment a slight respiratory acidosis which is completely physiological, and corresponds to
the last strong contractions, different is the situation where there is acidosis but the fetus is still high and has no
intention to go out.
If, on the other hand, the placenta is not functioning normally and/or uterine contractions are abnormal
(hypercontractility), the factors that improve fetal intrauterine oxygenation lose their effectiveness and the
factors that worsen oxygenation become more effective, therefore the balance from positive to negative and
this translates into increased fetal hypoxia (acute fetal suffering), a situation that must be resolved as soon as
possible.
Fetal hypoxia will first determine a respiratory acidosis (reversible) and then, due to the activation of anaerobic
glycolysis, quickly a mixed acidosis first and then more and more of metabolic type (irreversible), here that the
child may have problems for example is born non tonic, in cardiac arrest, and then during childhood could
reveal any problems for a possible previous ischemia.
The transition from aerobic to anaerobic glycolysis involves the fetus:
- the need to burn 19 times the amount of substrate to achieve the same energy response;
- the progressive accumulation of metabolic waste (ac. Lactic instead of CO2 and H2O) that is difficult
to dispose of through transplacental exchanges.
A fetus in acute fetal distress can be saved with childbirth and often and willingly if the situation is not
prolonged, it will not have any kind of problem. In contrast, if hypoxia started during pregnancy before the
onset of labor (chronic fetal distress), the fetus, in order to defend itself, implements the so-called "circulatory
centralization" or "preferential circulation" hypothesized by Saling.
Therefore, in the presence of chronic fetal suffering, the onset of labour in childbirth, even with normal uterine
contractions, can unbalance the existing balance and superimpose an acute hypoxia on the chronic one. For this
reason, when during pregnancy the presence of a functional insufficiency of the placenta and therefore chronic
fetal suffering is suspected, it is recommended to perform the Oxytocin test: the patient is administered, we
immediately see if the uterus responds well and contracts and especially if the fetus shows signs of fetal
suffering. If there is pain, the only chance you have is to do a C-section immediately.
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In this way, with the monitoring of labour in childbirth, on the one hand, the uterine contractile activity and, on
the other hand, the fetal conditions, I can see if fetal hypoxia arises. In this case, in order to avoid brain damage
or intrauterine death of the fetus, I must intervene immediately with a cesarean section.
In this way, modern obstetrics has the presumption of transforming such a dangerous journey, as the labour of
childbirth was defined, into a simple transfer in total safety of the new individual about to be born,
guaranteeing him/her the most preserved and intact potential for psychomotor development that he/she had
received in the genetic message inherited from the parental gametes at the time of fertilization.
This means that nowadays we have at our disposal all those facilities, machinery and medicines that allow us
to make sure that fetuses that cannot afford to make this trip do not do it, that fetuses that are sick during the
trip are pulled out and that fetuses that can afford to do it because they are well, because there is no acute or
chronic fetal suffering, because the size of the maternal pelvis is adequate do it essentially in total safety.
The term "labor monitoring in childbirth" generally refers to methods of monitoring fetal well-being during
labor. We have all the means to make the assessments, bring them back on the birth chart and make the best
decision based on the situation that presents itself. You have everything you need to face a difficult birth
(specifically, the professor refers to the gynaecology of Padua where there are midwives, gynaecologists,
anaesthetists, neonatologists, trainees, intensive care, dedicated operating theatres, etc.). The fundamental
concept is to direct the patient, with problems of various kinds, to the most suitable and equipped structure
possible in order to be able to follow her properly.
In this last part, the Professor resumed the monitoring very quickly because he had already dealt with it
previously.
The surveillance methods are biochemical monitoring and electronic monitoring with cardiotocography. This
track has two graphs, the upper one represents the fetal heartbeat, the one below the uterine contractions; when
looking at the tracks you have to check that there are spikes both above and below, indicating that the fetus is
moving; the baseline should be neither too high nor too low; I evaluate the contractions and their rhythm; the
decelerations of the heartbeat should be simultaneous with the contraction. He explained to us in previous
lessons how to interpret a track, i.e. whether a decrease in fetal CF can be dangerous or not depending on
whether it occurs before, after, or during the contraction.
AMENORREA
Amenorrhea: lack of menstruation. This is physiological at certain times in life, e.g. during pregnancy or
menopause.
The normal menstrual cycle is regulated by cyclic neuroendocrine mechanisms whose activity begins at
puberty and ends at menopause. These mechanisms are involved:
 The suprapotalamic system: regulates the secretion and release of releasing and inhibiting
hypothalamic hormones. It's governed by psychogenic, emotional, social and environmental stimuli.
In fact, above the hypothalamus there is the cortex which, for all intents and purposes, is the part
closest to our relationships, feelings and emotions (this is why it is said that a woman who has been
frightened by a car accident or had a strong emotion in a positive or negative sense, somehow
menstruation can stop, the hypothalamic signal in fact comes from above. The lack of menstruation
may last for a period.
 Hypothalamus centers: releases hormones to regulate pituitary gonadotropic gonadotropic activity

(GnRh) and integrates information from ovaries, pituitary gland and suprahypothalamus.
 Adenohypophysis: free FSH, LH and prolactin.
 Ovary: produces sex hormones (estrogen, progesterone and androgens). They are not produced
exclusively by the ovary but 50% of them are.
Menstrual cycle characteristics:
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- Must have a Rhythm: time between the beginning of two consecutive menses. It normally ranges from
24 to 32 days (on average 28 days). You can have them:
 Polymenorrhea: if less than 25 days (many menorrhoea in a year)
 Oligomenorrhea: if more than 36 days ( few menses in a year)
 Amenorrhoea: absence of menstruation which can be like this forever or only in certain
periods of life or even just for a month. But the real amenorrhea is the one that lasts at least 3
months, so if a cycle skips, it doesn't mean that there is something really important.
(definition of amenorrhea from the slide: absence of menstruation for at least 3 cycles or 90
days even if it is better to define it for at least 2 cycles or 60 days, if it is less
oligomenorrhea).
- The DURATION of a normal menstruation ranges from 3 to 7 days. Maybe:
 Extended: if longer than 8 days
 Short: if less than 4 days.
- The QUANTITY is normally between 25-80 mL.
 Hypermenorrhea: if it exceeds 80 mL (and if it continues like this it can become a
haemorrhage)
 Hypomenorrhea: poor, i.e. less than 20mL
 Menorrhagia: the loss that occurs during menstruation is more abundant and / or lasts longer
than normal flow (eg: if I have a very abundant menstruation that lasts me 10 days it is said
that you have a menorrhagia).
 Metrorrhagia: very abundant losses that appear in the interval between two menstruations or
in post-menopause. The loss could occur during the proliferative period or the secretive
period. E.g.: you can have an important blood loss that then stops, then another important
blood loss or simply you have a small blood loss every day, then it stops and so on, that is
more or less abundant blood loss that you can have in any period and not continuously from
the first to the last day of menstruation but rather 5 days, then it stops, 3 days and then it stops
etc..
Question 1: Is the amount of blood loss per single loss or in total? The answer is: in total. In case the amount
increases, the best thing to quantify the bleeding is to use a diaper, so not a tampax, because this way you can
see how much blood has been lost and how many times the woman needed to change it.
Question 2: What is the difference between hypermenorrhea and menorrhagia? Answer:. Menorrhagia:
abundant menstruation from the first day of menstruation for more than 7 days, hypermenorrhea means
instead that you have an abundant menstruation in the volumetric sense (over 80 ml). So menorrhagia is a
menstruation that lasts 10-15 days, hypermenorrhea can last 7-8 days but there will be an abundant loss of
blood. The two conditions intersect but it is important to understand if the condition is more of a "nuisance" or
a problem, i.e. if one has losses for 15 days it can be a nuisance but if it also loses 1L of blood in 15 days it is
no longer just a nuisance. Hypermenorrhea may well not be a pathology, simply the lady will have abundant
menstrual periods that disturb her life in those days and sometimes she may feel exhausted. So is
hypermenorrhea or menorrhagia better? Hypermenorrhea is better, it is more physiological, menorrhagia is
more of a problem because if you have 20-25 days of menstruation in a month it is more of a nuisance.
Hypermenorrhea can become a health problem while menorrhagia is more of a quality of life problem. (I find
this speech rather confusing.)
(From the Internet: menorrhagia is a term that indicates a particularly abundant and abnormal menstrual
blood loss; the bleeding can also extend beyond the physiological end of the menstrual period, which in the
presence of menorrhagia, in addition to being more intense, is often more painful.
Blood loss during menorrhagia can reach 80 mL with possible appearance of anemia. Menorrhagia should
not be confused with metrorrhagia: both conditions provide for hypermenorrhea, therefore abundant blood
loss, but while menorrhagia coincides with menstrual flow, metrorrhagia occurs between one menstruation
and another. A woman could still suffer from both conditions and there is talk of menometrorrhagia).
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Classification of amenorae:
 Physiological (prepubertal, pregnancy, menopause).

 Pathological, separated into:
Primitive: when a woman has never had and never will have her period (from slide: failure of
menstrual flow within 14 years in the absence of secondary sexual characteristics or within 16 years in
the presence of these).
secondary: disappearance of menstruation in a woman where there has been a more or less long period
of menstrual cyclicity.
Causes of amenorrhea divided by

compartment (from bottom to top):
 Uterus: 1 compartment
 Ovaries: 2 compartments
 Hypophysis: 3 compartments
 Hypothalamus, environment with
over-hypotalamic structures: 4
compartments
Any one of them could be the cause of

why.
1 compartment: uterus
 Asherman syndrome: A particular form that after an infection (e.g. very important endometritis)
causes the uterine walls to stick completely, so not only the basal layer is destroyed by this infection
and therefore there is no longer the possibility that there are receptors for sex hormones that allow the
endometrium to grow and flake every month, but in addition there are some sticky areas, so if you
wanted to go and have a look with a hysteroscope it would be difficult to stretch the uterus and you
would be faced with a real barrier. Then weir, the walls stick together and the basal layer is
completely damaged and does not respond to any kind of stimulus. You won't be able to get your
period because of a uterine problem.
From slide: Asherman's syndrome is a form of secondary traumatic amenorrhea characterized by the
presence of numerous sinecules that more or less completely obliterate the uterine cavity and/or
cervical canal as a result of scrapings or endometritis in which the exposure of more or less vast tracts
of myometrium leads to the formation of sinecules between the anterior and posterior walls of the
uterus.
A medical history and diagnostic hysteroscopy that reveals an absolutely inextensible uterus are
important for diagnosis.
The therapy essentially consists of hysteroscopic surgery with lysis of adhesions. They go to cut the
adhesions and clean the uterine cavity. This, however, only in some cases, i.e. when basically
somewhere the basal layer has remained. So the infection has led to the formation of these synaecules
that can be released, you can give metroplasty back a shape to the uterine cavity and you are lucky to
find a basal layer that can still react to sex hormones.
The teacher tells the story of an African girl who arrived in Italy and fled the war, her village had been
destroyed and she was raped several times by several soldiers. She had a serious infection, she could
not have children, at the first hysteroscopy she could not pass the internal uterine orifice, but with a
good hysteroscopist she was able to form a cavity, open the synaecia and give a shape to this uterus.
Then this uterus with the drugs started working again and the girl managed to get pregnant. This is
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because the surgeon also managed to preserve part of the basal layer with the possibility of being able
to respond to hormonal stimulation. It doesn't always turn out so well, though.
 Mullerian anomalies:
1. Hymen unperforated: it's the first thing you think of in a little girl. It's that little bandage of skin
that some woman has in her vagina and this can prevent the blood from coming out so that the
blood stays in the vagina. In this case simply go and break the hymen and immediately there will
be an emptying of the hematocut and then you will have regular menstruation without any
problem.
2. Obliteration of the vaginal orifice or interruptions in the continuity of the vagina lumen
3. Absence of cervix
4. Vaginal uterine agenesis
5. Congenital endometrial failure
As Muller's duct begins to develop and create the internal and external genitals, it is normal that there
may be some defect that alters these steps. These are rare anomalies.
Muller's ducts are two tubes which, with the atrophy of Wolff's ducts, in the embryonic life form the
two tubes in their external part, the uterus joining in the median part, the cervical canal and the vagina.
The errors in this process give rise to anomalies. Those listed determine primary amenorrhoea.
These are segmental abnormalities in the presence of a functioning uterus: adequately developed
subjects with normal secondary sexual characteristics, normal ovarian function, recurrent monthly
pain from hematocompulse, hematometry or hemoperitoneum. So we have people who have tubes,
ovary, hypothalamus, pituitary gland... who have everything perfect but the blood that forms, because
the uterus is normal and responds to stimuli, does not come out and then there will be amenorrhea
related to a problem of this type more or less serious, certainly the imperforated hymen is not a
worrying condition.
The therapy for the perforated hymen is very simple, it's a simple surgery. However, these women
with imperforate hymen can break it even during the first relationship. But most of them are girls who
arrive at the age of 14-15 years who may have had the telarca, pubarca at 13 and at 16 have not yet
had their period. They're girls who've developed but may not have had sex yet. These maybe go to the
doctor and at this point you can ask if the girl has ever had a relationship, if the answer was no, you
can look for this little barrier.
The therapy is surgical with restoration of normal patency of the genital canal.
 Agenesie Mulleriane: Rokitansky syndrome (absent or rudimentary vagina).
Rokitanski's syndrome: total absence or hypoplasia of the vagina, so we are dealing with women with normal
but lumenless or rudimentary uterus with the presence of two distinct cords. They have normal ovarian
function, with preserved ovulation and normal somatic development.
Diagnosis: clinical examination and execution of the karyotype to exclude a pseudohermaphroditism,
radiological examinations are performed where they can be frequently found in this ectopic kidney syndrome,
horseshoe kidney or ureteral abnormalities.
Therapy: create a vagina mole, create a gap between the urethra and anterior rectal wall and place a phallus-
shaped vaginal dilator.
Once, instead, Vecchietti's olive was used. Vecchietti was the director of the clinic in Padua until about '65 and
for these girls he had designed an instrument that was slightly inserted into the vagina (often these girls had
about 1 cm of vagina), he put a small metal olivette and once positioned, he would stretch this olive with an
instrument bringing the olive further and further forward, the pz would adjust itself in order to create this
neovagina.
Now instead, dilators are used which are kept inside and slowly go to make this vagina have a pseudonormal
size.
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The vagina of a normal woman is between 8-12 cm, these women may not reach 8 cm but they can reach the
right cm to have a normal sex life.
2 compartments: ovaries
On the hormonal level there is a deficiency of steroid hormones, in particular estradiol, and with an extremely
high secretion of gonadotropins (hypergonadotropic hypogonadism).
These women are particularly unlucky because they have a deficiency in the hormones that make them feel
good, e.g. estradiol. Estradiol makes you feel good, makes you beautiful.
Could be:
 Primary: there is a malformative or dysgenetic state so important as to prevent pubertal development:
1. Turner's syndrome or mosaicism
2. Testicular feminization (Morris syndrome)
3. Swyer syndrome (gonadal dysgenesis XY)
4. Agenesis gonadica
These women do not have ovaries, therefore they do not produce eggs and this is linked to fertility, moreover
they do not produce estrogen so the endometrium will never react, will grow, will never flake and you will not
have menstruation.
 Secondary: if the congenital or acquired gonadal disease leads to the functional deficit of the organ
only in a more or less long time after the menarche.
1. Resistant ovary syndrome
2. Early Menopause
3. Gonadal agenesis on a nongenetic basis, it is usually very difficult to have gonadal
agenesis on a nongenetic basis of both ovaries, it is much easier to find patients with only
one ovary.
Turner syndrome
The most famous syndrome of compartment 2, is a syndrome that is characterized by a non-normal karyotype
(X0). In 80% of cases you have 44 plus X0, in 20% 44 plus translocation or deletion Xx or mosaicism X0/XX.
It is a genetic-based disease and occurs on 1/10 000 female infants, so it is not so unusual.
The clinical picture is characterized by almost non-existent levels of estrogen with the absence of negative
feedback on the hypothalamus pituitary and FSH axis which rises at puberty to the typical values of
menopausal women with consequent sexual infantilism and streak gonads (i.e. the ovaries exist but are
elongated fibrous bandages with no primordial follicle inside).
They are women easily recognizable by their physical appearance: short stature (140 cm, due to abnormal
cellular response to IGF1), typical facies (micrognathia, epicantic folds, low hairline and eyelid ptosis), shield
chest with microtelia, short and wide neck with low hairline, pterygium of the neck, cubitus valgus, excessive
number of pigmented nevi, tendency to the formation of keloids and hypoplastic nails.
They are women who may also have cardiovascular or renal abnormalities (from slide: cardiovascular
abnormalities such as aortic coarctation, renal abnormalities e.g. kidney rotation, horseshoe kidney,
hydronephrosis secondary to ureteral obstruction, lymphedema of feet and hands, arterial hypertension, severe
form of post-menopausal osteoporosis).
Diagnosis: the suspicion is in the presence of amenorrhea, based on the statural delay and appearance of
somatic stigmata. Definitive diagnosis with karyotype.
These women can't have children.
Treatment: estrogen and progestin replacement therapy from age 12.
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You can also have a hypoplasia of the small lips,

but the vagina is present so it is a woman who can
safely have sex.
Morris syndrome:
male pseudohermaphroditism known as beautiful woman syndrome.
The professor tells of two sisters that he himself had operated on who were beautiful and nice girls, they
underwent surgery and then psychological support but had a normal life even if without ovaries.
The karyotype is XY, but there is an anomaly in the androgen receptors that causes a receptor transmission
insensitivity with recessive X-linked gene, which is why they have no hair and no male traits.
Phenotypically female subject, with female external genitalia, short blind bottom vagina and absent Mullerian
structures. The testicles are believed to be in the large lips/inguinal region (incomplete PAIS form where the
receptors function partially) or in the abdomen (complete CAIS form where there is complete absence of
testosterone action) and have few spermatogons and spermatogenesis absent and predisposed to neoplastic
degeneration (these testicles should be removed because, due to the temperature in the abdomen, they can
degenerate neoplastically).
In adolescence, secondary female sexual characteristics develop, but amenorrhoea and absence of the hair
system make them worry and go to the paediatrician or gynaecologist.
Endocrine Quadra endocrine: testosterone and LH levels are higher than normal due to absence of negative
feedback to LH; normal FSH level; estradiol levels are high for peripheral testosterone conversion and direct
testicular production. However, they are women who look completely feminine, often beautiful, with beautiful
breasts, beautiful hair, beautiful skin, but they need to be operated on.
Question 1 from a student: Has it ever happened that when these girls discover that they have a karyotype XY
someone risks adopting a male appearance. The professor answers that he has no experience in this matter,
usually they are pcs that are operated on and then sent to a psychologist but then they are pcs that have little
need of the gynaecologist because they have no uterus or ovaries, so they are lost. The vagina can also be very
short and can partly solve the problem with a vaginal dilator or transplant, but it is difficult to have a normal
life, you cannot have children and sexual intercourse is often not optimal.
Question 2: when talking about Rokytansky syndrome, there was talk of the possibility of recreating the
vaginal canal as it may be absent while for women with Morris syndrome this intervention is planned or is it
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an option? Answer: Rokytansky is a pathology of compartment 1 so it essentially means vagina and uterus and
these are pz that basically the vagina does not have it and therefore it must be reconstructed.
Morris syndrome, on the other hand, is a pathology that in reality many times has a vagina even human type 3-
4 cm, which is acceptable. So you can do something in both, but they are two different conditions.
The student refers to the case told by the teacher of a girl with Morris syndrome who is discovered because she
cannot have sex and her vagina was 1cm, the psychological impact was important. At this point the teacher is
asked if it would be better to intervene and he replies that he is not a psychologist. But he also says that
sometimes some of these women make a neo-vagina with the intestine, the work is usually quite satisfactory,
the only problem is that the vaginal odor is not very good but as a fit for a penis can also go well and from the
point of view of sexual pleasure is quite good because fortunately sexual pleasure is mostly related to the
vulvar host and the first third of the vagina rather than the last portion. So they can have pleasant sexual
intercourse.
A very general discourse on the figure of the psycho-sexologist and its importance begins, but the professor
says he is not particularly expert in this field, he says he is more of a practical man.
Diagnosis: suspect based on clinical picture (glabrous subject with amenorrhoea and blind bottom vagina);
definitive diagnosis with karyotype.
Therapy: gonad ablation and estroprogestin replacement therapy.
Most have testicles in the abdomen that can

be easily removed laparoscopically. Some of
them have special prominences. The vagina
is small and everything else is missing.
Swayer syndrome:
male pseudohermaphroditism. The karyotype
is XY.
The syndrome is linked to X or autosomal
dominant defect with alteration of the SRY
antigen.
The subject is phenotypically female, has a
vagina with a blind bottom (but it is
complete) and uterus and tubes absent (she
has no menstruation and no ovaries), the
gonads look like streak gonads (fibrous
cord), so they are not as lucky as the Morris
which have the androgens produced by the
testicles that are then converted into estrogen,
and have a very high risk of malignant
degeneration and must be removed.
Morris are females in the head and in the body and are beautiful because they produce estrogen, when they go
to remove the testicles they will miss the androgen-estrogen conversion and so they have to do estrogen
replacement therapy as long as possible, potentially for a lifetime although this can be a risk factor for some
tumors and then evaluate what to do. Someone claims that in a pz with Morris syndrome, after removing the
mammary gland, you can use estrogen forever since it has no uterus or breast.
Question: Does the therapy scale in time or does it take off at some point? The teacher says he doesn't have
much experience in this field, personally the teacher would keep it up until the pz is well and then with time
maybe go climbing. Estrogen makes her feel good not only physically but also in her head.
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Gonadal agenesis on a nongenetic basis:

generated by viral diseases (parotitic ovaritis), autoimmune ovaritis or metabolic deficiencies in early
pregnancy. There are no particular clinical problems other than hypergonadotropic hypogonadism.
Hypogonadism for streak gonads and you have hypergonadotropy, the pituitary gland produces FSH, does not
find the function of estrogen and FSH rises, you try to stimulate the ovary then but the ovary does not respond.
Resistant ovary syndrome (Savage syndrome):

probable presence of ovarian ab antireceptors for gonadotropins. FSH and LH elevated in association with
marked hypoestrogenism.
The ovaries have a normal heritage of primordial follicles but without further development.
The diagnosis is made by evaluating the endocrine picture and with ovarian biopsy.
Therapy: in exceptional cases it is possible to induce ovulation using a combination of exogenous high-dose
gonadotropins and GH. Since primordial follicles exist, in some cases they can grow and develop.
Early menopause:
detection of repeated dosing of high FSH levels before 40 aa.
Etiology: genetic disorder in 10% of cases (45X, 47XXY, MOSAICISM, X fragile). In 2/3 of cases the cause
remains unknown (viral, chemical, physical or autoimmune etiology). Eastern Europe is most frequently
affected by this problem.
The clinical picture is characterized by oligomenorrhea with anovulatory cycles up to secondary amenorrhea
before age 40, infertility, mood disorders, estrogenic and androgenic deficiency disorders.
Diagnosis: ovarian biopsy with evidence of albicant bodies testifying to previous ovulations and absence of
residual follicles as in menopause.
Therapy: estroprogestinic.
FAMILY PLANNING
DEFINITION
Family planning makes it possible to decide whether to procreate through complete relationships or not,
using a temporary prevention, limited in time, of the onset of a pregnancy by pharmacological,
mechanical, behavioral means. Today we have understood how the ovary works and how it is regulated
by the pituitary gland and hypothalamus.
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The purposes of contraception are:

 Prevent the production of gametes
 Prevent fertilization
 Prevent nesting in utero
There is also sterilization planning, i.e. permanent prevention of pregnancy.
The choice of prevention mode must be made according to the patient's needs, evaluating:
 Effectiveness and convention of the method
 Risks and associated benefits
It is also necessary that the patient is properly informed and the choice is shared.
IDEAL CONTRACEPTIVE
An ideal contraceptive should be:
• 100% effective
• Innocuous
• Free of side effects
• Reversible
• Easy to use
• Accepted by the patient
There is no ideal contraceptive method, as it is practically

impossible to reach 100%, what is used to assess the effectiveness
is the Pearl index (ideal when it is <1); this parameter is nothing
more than the number of unplanned pregnancies that have occurred
during a certain period of time (1 year) in 100 women who have
correctly used the contraceptive method under examination.
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The pill has a Pearl index of 0.07-0.5 (<1) and is very effective. The IUD and the minipill have a higher
index and are therefore less safe. Other methods, such as interrupted coitus (10-50) are not effective.
NATURAL METHODS
WHO defines them as methods for planning or avoiding pregnancies based on observation of the natural
signs and symptoms of the fertile or infertile phase of the menstrual cycle. The biological preconditions
for such methods are:
 the ability to fertilize gametes limited in time: 6-12 hours for the egg and 3 days for sperm;
 one ovulation per cycle;
 determinability of the ovulation date.
Among the natural methods, which can also be used to plan a pregnancy, there are:
 Ogino-Knaus method, which, according to Ambrosini, has given many unwanted children and
which consists in abstaining from sexual intercourse during the days with more probability of
fertilization. The Japanese Ogino, in fact, has established that ovulation takes place between the
16th and 12th day before the start of the next menstruation. Assuming a maximum spermatozoa
life span of 3 days, the fertile period from the 19th to the 12th day before the next menstruation is
deduced. In the case of a woman with a normal menstrual cycle of 28 days, the fertile period is
between the 10th and 17th day of the cycle. In practice, however, in most women, the duration of
the menstrual cycle is irregular or different from the indicative 28-day period; in these cases the
fertile period can therefore fluctuate unpredictably, making the application of this method
difficult as well as ineffective (in fact, the Pearl index is high).
 Basal temperature: progesterone, which is the master in the second phase of the cycle, is
thermogenetic. Then by measuring the temperature daily, it is possible to determine the date of
ovulation with an accuracy of ± 1-2 days. Ovulation is considered to have occurred when an
increase of 0.3-0.5 degrees is observed. You must abstain from sexual intercourse from 3 days
before to 3 days after the temperature rise.
 Billings method: it consists in determining the fertile period by observing the cervical mucus,
which becomes more fluid and elastic near ovulation, to facilitate the sperm path. Prevention is
implemented by abstaining from sexual intercourse during the fertile period. It is not a very
reliable method because, besides requiring a programming of the reports, it requires the
microscopic observation of a mucus called "fern
leaf".
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 Person: consists of a contraceptive system which, by monitoring hormone levels, is able to

determine what fertile days are. Basically, with simple disposable sticks it analyzes the morning
urine and signals on a small portable monitor if you can have sex.
BARRIER METHODS
They have a mechanical action, they prevent the penetration of spermatozoa into the cervical canal or
vagina. They do not require medical intervention, protect against sexually transmitted diseases and do not
have the side effects of oral contraceptives or spirals.
They are:
 Condoms
o In addition to avoiding unexpected pregnancies, condoms protect against sexually
transmitted diseases (HPV, HSV-2, Chlamidya, Gonococcus, CMV, HIV). There is a
50% reduction in the risk of transmission.
o Has a 3.5% failure (if used incorrectly or broken)
 Diaphragm
 Cervical hood
 Vaginal sponges
 Spermicides
INTRAUTERINE DEVICES
It is a device made of plastic material (polystyrene), coated with
radio-matt material (barium salts), with various shapes (T-
shaped, Y-shaped, semi-circular). They are coated with copper,
silver or progestin to increase effectiveness and have a duration
of 5-7 years, generally 4 years. They have a protruding thread in
the vagina, which allows them to be removed.
There are Asian devices, mostly Chinese, which are difficult to extract
because they are not equipped with wire. They are inserted using a
spring mechanism: they are compressed and then released into the
uterine cavity. This, in addition to the difficulty in removal, also leads to
inflammatory reaction and possible fusion with the mucosa.
Once the instrument is placed inside the uterus, it creates a sterile intracavitary inflammatory reaction
(foreign body reaction) throughout the endometrium, releasing toxic cytokines for sperm and blastocyst
and modifying tubal motility (it does NOT act as a barrier!).
It is essential to sterilize the device prior to insertion, to prevent uterine infection, which can have even
very serious long-term consequences, such as permanent sterilization (Asherman's syndrome =
obstruction of the uterine cavity by scar tissue with formation of fibrotic adhesions that prevent the
nesting of the product of conception). In fact, there is always a tendency to give antibiotic coverage the
day before and the days after the device is introduced. It is preferably applicable during the flow, after
exclusion of an ongoing pregnancy, even after childbirth or abortion (increased risk of expulsion in the
following six months). It can be removed at any time, with immediate resumption of fertility; a new
insertion is possible immediately after antibiotic therapy.
The risk of pregnancy is around 2-3% during the first year, then gradually decreases. If this were to
happen and the IUD was extra-amniotic, it would be possible to continue the pregnancy, but it would
increase the risk of abortion. If the thread is clearly visible in the vagina, it should be removed. In case of
infection, IVG (voluntary termination of pregnancy) is indicated due to the risk of maternal sepsis.
Side effects:
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 infections with anaerobic vaginal flora at insertion; symptoms appear after 3-4 months:
abdominal pain, modest fever rise;
 bleedings;
 possible disturbance during intercourse (due to the thread that is deliberately left to come out of
the external uterine orifice by a couple of centimetres to allow removal).
Contraindications:
 PID (Pelvic Inflammatory Disease) in progress or previous;
 hypermenorrhea, menorrhea, dysmenorrhea;
 uterine malformations;
 submucosal fibroleomyomas;
 anticoagulant therapy;
 immunosuppression;
 Allergy to copper, Wilson's disease (this contraindication applies only to the instrument
containing copper);
 risk factors for endocarditis (if there is only valvular prolapse, prophylaxis at the time of insertion
is sufficient).
ORAL CONTRACEPTIVES
 Estro-progestinics (pill)
 Progestinics (minipill)
 Emergency contraception (morning-after pill)
 Progesterone Antagonists (RU 406)
ESTROPROGESTINICS
The estrogen used is ethinylestradiol in association with different progestins (Levonorgestrel,
Ciproterone acetate, Desogestrel, Drospirenone, Gestodene) and have different properties. For
example, if you want to move more towards an anti androgenic action because the patient has some
problem related to seborrhea (acne or comedones) or hypertrichosis, you prefer to use Ciproterone acetate
(Diane). Drospirenone, on the other hand, has a lower mineral-corticoid action than the others.
It is considered the best method of contraception for young women, thanks to its high effectiveness
(almost 100%) and the presence of many additional benefits:
 reduces irregularities in the menstrual cycle;
 reduces menstrual pain;
 reduces premenstrual symptoms;
 fights acne and oily skin;
 fights excess hair;
 protects against the formation of ovarian or breast cysts (particularly useful effect in women with
polycystic ovary syndrome).
You have to take one pill a day, always at the same time. After 21 days of intake (in some cases after 24),
the estroprogestin pill is suspended or replaced with a placebo for 7 days (4 days for 24-day pills). During
this interval the so-called "suspension bleeding", similar to a menstruation, should occur. After 7 (or 4)
days, the pill is taken for a new cycle. The first pack should be started on the first day of menstrual flow,
the following ones, respecting the 7-day break if that type of pill provides it (which means that if there are
still blood leaks, but the 7-day break is over you take the pill anyway). This is because the FSH share
starts to increase due to negative hormonal feedback already in the desquamative phase, when estrogen
levels are low. Therefore, taking contraceptives on the first day of menstruation immediately stops the
pituitary production process of FSH. If you take the first pill on day three, for example, FSH levels may
already be high enough to allow some follicles to mature.
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The first generation pills had 50 ugr of EE, the second generation pills had 30 ugr of EE, the third
generation pills that we currently use have 20 ugr of EE. EE cannot be completely eliminated because of a
pituitary feedback problem.
The pills can be

 Monophasic, i.e. a pill in which the dose of EE and progesterone is always the same for all days
of the cycle
 Biphasic, i.e. pills that have half a cycle with one dose and half a dose with another
 Triphasic, has different dosages in the first third, second third and last third.
The mechanism of action is to block ovulation, which is suppressed from the first cycle of intake by
inhibition of gonadotropin secretion. In particular, progesterone suppresses LH and its peak by preventing
ovulation, while estrogen suppresses FSH by preventing follicle selection and emergence dominated. In
patients using the pill we observe a modification of the cervical mucus and a decidualization of the
endometrium.
In case of forgetfulness, the procedure to follow varies whether or not more than 12 hours have elapsed.
Safety is not guaranteed if an episode of vomiting or diarrhoea occurs immediately after intake (within 3
to 4 hours), so there is a tendency to advise the patient to take another tablet immediately afterwards, or to
pay special attention to sexual intercourse until the end of that cycle, because it may not be fully covered.
The most common side effects are:
 nausea;
 breast tension;
 headache;
 possible weight gain;
 mood swings;
 possible decrease in libido is very difficult for this to happen in a young patient, but it must be
borne in mind that the pill is also used in women who are in the first stage of menopause before
moving on to more specific therapies, and in the latter case the decrease in libido is much more
frequent.
First visit to prescribe CO

In the medical history it is important to ask if the patient suffers from (or if there have been cases of) deep
vein thrombosis, stroke at an age <50 years, abnormal haemostasis, hypertension, dyslipidemia or
diabetes. Haematochemical checks are performed after 3-6 months (cholesterol, triglycerides, blood
glucose, coagulation, liver function) and then every 5 years if no complications occur.
Contraindications
Absolute:
 thrombophlebitis and thromboembolic diseases;
 genital bleeding of undiagnosed;
 liver cancer (both benign and malignant);
 breast cancer.
Relative:
 smoking, hypertension, cerebrovascular disease;
 severe headache and depression;
 cholelithiasis;
 severe acne;
 liver enzyme-inducing drugs.
Isn't the pill also used for acne?
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It is used for acne because it prevents androgens from over-stimulating the pilosebaceous unit. But severe
acne can be due to high levels of androgens not necessarily produced at the ovarian level but also at the
adrenal level. It may also be due to colonization by bacteria (staphylococcus) of the pilosebaceous unit. In
this case antibiotic therapy is used. Even a liver deficit (the liver produces SHBG) can give acne.
So it is important to assess the form of acne and choose the most appropriate therapy.
Why can't it be administered in patients with severe depression?

Estrogens are the "natural female doping" and lead to an improvement in mood. Yasmin, much used
because it has very low levels of estrogen, does not make you fat, in predisposed women it gives a change
of mood and a lowering of libido.
Thromboembolic risk
The thromboembolic risk is increased by the use of CO and the RR is lower in 2nd generation CO (3.2)
than in 3rd generation CO (4.8). Some genetic variants of the coagulation factors, such as Leiden's factor
V mutation and the factor II variant predispose to TV and, in association with CO, give an important
increase in risk.
Blood pressure
Estrogens increase renal activity and therefore pressure, which must be measured every 6 months. High-
dose CO gives 5% PA increase. Any increase in pressure will disappear within a few weeks of
suspension.
Interferences
EPs lead to:
 enzymatic induction at liver level with faster elimination of steroids
 increase in SHBG levels with decrease in the amount of free active hormones
Estrogens may increase or decrease the effect of other drugs
EP and neoplasms
EP can increase or decrease the risk of developing certain neoplasms.
 Udder cancer, there is an increase in risk, but this risk gradually decreases in the following years
to zero one year after suspension. If the pill is taken at the age of 20 you can rest assured, if it is
taken at the age of 45 it is good to do some checks.
 Cervical neoplasia with increased risk of dysplasia and K in situ after 1 year; risk of K increases
2-fold after 5-10 years; risk of cervical adenocarcinoma doubles after 10 years. Periodic checks
with PAP tests are necessary. The reason is the non-use of the condom and the consequent
increased risk of HPV.
 Endometrial neoplasia: there is a 50% reduction in risk after 12 months, with greater effect in
nulliparous and low-equal women.
 Ovarian neoplasia: there is an 80% reduction in risk after 10 years of developing epithelial K.
Women who use the pill and block ovarian function are more covered for this tumor.
MINIPILLOLA
It consists only of progestin, has no significant metabolic effects and is sometimes used during lactation.
As side effects it presents:
 high frequency of bleeding;
 menstrual irregularities;
 formation of ovarian functional cysts;
 lower contraceptive safety than estro-progestin pills (the Pearl index is 1.5-6).
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PROGESTERONE ANTAGONIST (RU 486 MIFEPRISTONE)

It acts through competitive interaction because it has high affinity with the endometrial progesterone
receptor and prevents nesting, interrupting the initial pregnancy. The administration of the so-called
"morning-after pill" leads to a modification of the endometrial substrate during the reproductive window.
It is given after sexual intercourse and must be hired as soon as possible. The probability of success is
very high if taken within a few hours, after 72h the effectiveness decreases rapidly.
In addition to RU 486, emergency contraception can be done with:

1. Progestin (Norlevo) 1 tablet containing 1.5 mg of the hormone should preferably be taken within 12
hours of the risk report, but no later than 72 hours. Editor's note. Since 2009, in addition to Norlevo,
which is based on levonorgestrel, there is also EllaOne: a drug based on ulipristal acetate (a selective
modulator of the progestin receptor that is able to move ovulation) which, although it is preferable to
take it as soon as possible, is effective up to 120 hours (5 days) after the risk relationship. Source: Core
Curriculum Gynaecology and Obstetrics, Ferrari and Frigerio; drug data sheets).
2. Progesterone releasing IUDs can be entered even 5-7 days after the report.
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VAGINAL RING
Made of biocompatible, flexible and transparent material, it should be introduced
into the vagina. It contains estrogen and progestin which are released daily at fixed
rates. It should be left in vagina for 3 weeks and then removed. After a suspension
of one week, a new one must be inserted. The mechanism of action of the ring is
comparable to that of the pill.
The absolute contraindications are:
 severe vaginal prolapse (difficult in a young woman)
 Urinary incontinence
 Vaginal or urinary infections
 Dispareunia
It does not undergo first pass metabolism and has no impact on the stomach, i.e. there are no problems of
lack of absorption in case of vomiting/diarrhea.
The side effects are:
 Alterations in the menstrual cycle
 vaginal discharge (more frequent in the first 3 months of application);
 possible disturbance during intercourse (rare)is practically impossible for the partner to feel it
because it goes around the cervix.
 accidental loss (rare).
MALE STERILIZATION: VASECTOMY

It is performed under local anesthesia, with a small scrotal incision and subsequent closure of the deferent
ducts through ligatures, cutting and introflection of the stumps.
The failure of the surgical procedure is 3-4 patients out of 1000 interventions.
Complications are local infections and coagulopathies.
The success rate in case of recanalization is 37-90%.
FEMALE STERILIZATION: TUBULAR

There are 3 methods:
 Laparoscopic where either electrocoagulation is performed with bipolar pliers or silastic rings,
titanium clips coated with silicon rubber are applied. Bankruptcy is 1-3/1000
 Mini laparotomy that is performed in a non-obese patient who has not undergone previous
abdominal surgery and consists of making a suprapubic incision and continue with the Pomeroy
method (removal of a section of the tuba). This is the method most frequently used, especially in
the United States, as it is simpler and faster. When the abdomen is open, the tuba is grasped and
lifted in the median section with a haemostatic clamp and the loop that forms in this way is
perforated, tied and then resected, with removal of at least 2 cm of tuba.
 Hysteroscopy (HSC) carried out to place silicone caps in the tubal hosts with good tolerability
and good reversibility.
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UTERINE FIBROIDS
The leiomyoma/fibroma/ uterine myoma is a benign tumor that originates from the muscle tissue of the
uterus that is most frequently found in gynecological pathology. In some cases it is necessary to remove
them and in others they can be left in place.
The characteristics of fibroids are:

 frequency between 25-50%, 30% in patients of childbearing age
 age most susceptible to the development of uterine fibroids between 30 and 50 years of age
 the black populations are particularly affected
 growth and increase in size during pregnancy (in these cases a removal surgery must be
performed if the patient wishes to become pregnant)
When a patient presents with a fibroma, it's important:

- assess where the fibroma is located
- assessing the volume of the fibroma
- measure the age of the woman
- check for symptoms
- investigate the patient's expectations (since a myoma can be a problem for a woman who wants
children, whereas it may not be a problem for a woman in menopause).
Epidemiology
- The disease affects 25-50% of women of reproductive age (between 25 and 45 years) and their
incidence increases with age.
- Post-mortem studies have found an incidence of up to 77%.
- Myomas are present in 5-10% of infertility cases.
- The incidence in infertile patients in the absence of other known causes of infertility is between
1-2.4%.
- The incidence in pregnant patients is 1.4-8.6%.
Classification
A fibroma can be classified according to:
 Location: in this case you have fibroids:
- Subserositis: under the visceral peritoneum, they can be
 sessile
 pedunculate
- Intramural: in the thickness of the myometrium
- Underucosis: protrudes into the uterine cavity and causes

distortion, they are distinct in
 Type 0: stems without extension
intramural (protrude entirely in
hollow)
 Type 1: sessile with intramural extension <
50%.
 Type 2: with intramural extension > 50%.
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- Fractional: they develop from the lateral uterine wall, are more frequent in the istmic area, do
not distort the uterine cavity and protrude towards the serosa by less than 50%.
 Number: in this case you have fibroids:
- Singles
- Multiple (uterine fibromatosis)
 Localization:
- Uterine body (95%)

- Uterine neck (5%)
 Size
- By a few millimeters
- Several centimeters (even >20 cm)
Risk factors
- Familiarity: RR is 3.47 if positive family history is present
- Ethnicity: in black women the diagnosis of myomas occurs at a younger age and in greater
numbers.
- Nulliparity (the relative risk decreases by 20% per birth to 0% after 5 births)
- History of infertility
Protective factors
Pregnancy is a protective factor. Even if a fibroma can grow during the first months of gestation, being a
tumor that "feeds" on estrogen and the ovary being at rest during the nine months, there is not the
production of estrogen necessary for the growth of new fibroids, consequently we can deduce that during
pregnancy pre-existing fibroids can grow and new ones cannot be formed. In addition,
during pregnancy the chance of fibroids forming decreases:
- loss of small fibroids during puerperal involution
- the effect of transient zonal ischemia during remodeling
Pathogenesis
They contribute to the development of a two-component uterine fibroma:
1. genetic component:
- leiomyoma can originate from the growth and proliferation of a single smooth
muscle cell (monoclonal theory)
- about 20 - 50% of uterine myomas have chromosomal rearrangements
- studies at the molecular level have shown 226 genes with altered expression in
leiomyomas:
 152 down-regulated (TRAIL) with role in activating apoptosis
 74 up-regulated (TGFb1, PDGFc, IGFbp6) involved in proliferation
mobile phone
2. hormonal component: all situations of hyperestrogenism can facilitate the growth of fibroids
because the pathology itself is estrogen-dependent. The association between fibroma and
estroprogestinic hormones is also confirmed by the fact that:
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- incidence increases in fertile age

- fibroids are stationary or in involution with menopause, they often become small and
calcify.
- the fibroma often has an increased expression of enzymes that convert
androstenedione to estradiol
- the fibroma increases in size during pregnancy, also due to increased HPL (placental
estrogen)
- there is frequent association with endometrial hyperplasia
- progesterone seems to inhibit its growth
- there is braking action by the GnRH
In general fibroids can lead to:
 Anatomical alterations (may prevent the migration of gametes, embryo and damage the blastocyst
implantation)
- Deformities of the uterus
- Enlargement, elongation and cavity distortion
- Obstruction of tubal hosts or cervical canal
 Functional alterations (hinder the transport of gametes and the implantation of the blastocyst)
- Alterations in uterine contractility
 Endometrial thinning or atrophy

 State of chronic inflammation
 Focal alterations of vascularization and secretion of vasoactive substances
 Endocrinological changes in the endometrial environment with increased androgen secretion
(hinder the implantation of the blastocyst)
Speed of growth
The difference depending on the individual case: in some patients the myoma can keep the same volume
for years or grow slowly, in others it can become large within a few months.
Macroscopic anatomy
The consistency of the tumor may be:
- Hard: for more fibrous component (the most frequent)
- Springs: for greater muscle component (colliquated fibroids)
From the point of view of colour the fibroma can occur:
- White: for more fibrous component (more frequent)
- Red: for more muscle component
The mass can be characterized by a pseudocapsule, a thick layer of clear areolar connective tissue
compressed by the tumor expansion (it benefits the surgeon during the removal as it allows to remove the
fibroma easily sparing the muscle tissue).
In adenomyosis, on the other hand, there is no pseudocapsule and healthy muscle tissue is also removed
during removal.
Symptomology and clinical picture
The symptomatology is affected by:
 volume
 number
 location
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A fibroma can be:
 asymptomatic: in 50% of cases, in fact, the majority of women do not know they have a fibroma
and do not have any type of symptoms.
 symptomatic: in this case it can give

- pain or weight gain
- infertility
- preterm delivery and pregnancy pathology (placenta previa, placenta detachment,
abnormal presentations, dystocia, abnormalities of seconding and postpartum)
- leucorrhoea (increased secretion of the vaginal glands due to uterine congestion, the
liquid produced is whitish and creamy)
- menometrorrhagia (pathological increase, in quantity and duration, of menstrual flow;
there is also the inability of the uterus to contract regularly at the end of menstrual flow
and uterine and pelvic congestion; the hyperestrogenic endometrium assumes
hyperplastic characters with areas of necrosis and interstitial hemorrhages that cause
menorrhagia)
- metrorrhagia (intermenstrual blood loss that can be due to submucosal fibroids that
ulcerate)
- anemia (resulting from menorrhagia or metrorrhagia)
- compressive symptoms at the level of:
 bladder: with chickenpox, urgent urination, urinary retention
 ureter: with hydronephrosis
 rectum: with constipation and sub-occlusions
- pain due to:
 contractions of myometrium in an attempt to expel the mass (similar
pain
to menstrual pains)
 compression phenomena on the various organs or adhesions with
omentum and
intestine
 twisting on the pedicle of the fibroma with subsequent necrosis
 necrosis or suppuration
 endometriosis
- effects on the patient's quality of life (patients not eager for offspring)
Modifications to the structure
A fibroma can go to:
- Hyaline degeneration (60%, especially post-menopausal)
- Cystic degeneration (4%)
- Calcification (in older women)
- Fat degeneration
- Sarcomatous malignant degeneration (0,1-0,2 %).
Diagnosis
You have the diagnosis at your disposal:
- clinic (medical history, gynaecological examination)
- ultratomography
- hysteroscopy
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- 3D hysterosonography
- laparoscopy
- TAC / MRI
- Hysterosalpingoscopy
- cystography, urography, opaque clisma (performed only if the symptomatology reports
problems of
compressive type)
Therapy
Myomas don't necessarily have to be treated because:
- the incidence in pregnant patients is 1.4-8.6%.

- only 10-20% of pregnant patients with fibroids experience complications (IUGR, preterm birth,
poor presentation) during pregnancy
- in 80% of cases the myomas remain the same size or even regress during pregnancy.
- patients with 3 cm myomas have no risk of complications during pregnancy.
- can be intramural and not give distortion of the uterine cavity
- may have dimensions < 5 cm or be multiples of dimensions < 2.5 cm without cavity
involvement
- surgical therapy and PMA present risks, particularly the latter can give:
 ovarian hyperstimulation syndrome (8-10%)
 mild grade (8-20%)
 moderate grade (0.5-7%)
 severe grade (0.6-2%)
 Acute abdomen from anxial torsion (0.1%)
 operator risks related to oocyte sampling (pelvic infections 0,8% and
hemoperitoneum 0.07%)
 miscarriage (15-30%)
 ectopic (2-8%) and heterotopic (1%) pregnancies
- myomectomy
 laparotomy presents:
 risk of recurrence of 50% at 5 years of age and 27% at 10 years of age
(the number of myomas
is related to the frequency of recurrence)
 risk of a second intervention varying between 11% and 26%.
 3-8% risk of hysterectomy
 0.002% risk of rupture of pregnant uterus
 94% risk of post-surgical adhesions in case of wall incision
rear uterine, in 56% in case of anterior uterine wall incision
o fundica with increased risk of ectopic pregnancy and worsening
infertility
 laparoscopic presents:
 1% risk of rupture of the pregnant uterus
 laparotomic conversion rate of 2-10%.
 2-6% risk of hysterectomy
 post surgical adhesions in 35%.
 recurrence at 5 years of age up to 50%.
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 hysteroscopic presents:
 20% recurrence at 5-10 years of age
 risk of hysterectomy 0.5-12%.
When to bargain?
The treatment is necessary in the case of submucosal myomas as it is well known that they decrease
fertility and their removal improves pregnancy rates. In the case of intracavitary and subserositic
myomas, studies have shown a decrease in reproductive function and shown a benefit in performing a
hysteroscopic myomectomy.
Myomectomy for prophylactic pre-PMA purposes, in asymptomatic patients with normal uterine
cavity, is not only unjustified, but can be detrimental to reproductive function: in patients with
subserositic or intramural myomas, who have no uterine cavity deformities and size < 5 cm, in the
presence of other causes of infertility, the first approach is PMA.
Myomectomy as a first approach should be performed in case of:
- uterine cavity distortion

- large myomas regardless of the distortion of the uterine cavity (the limit size that justifies
intervention is 5 cm)
Medical Therapy
Useful to control fibroma-related disorders (menometrorrhagia and dysmenorrhea).
It's more effective for intramural myomas and subsierositis.
The drugs that are used are:
- synthetic GnRH analogues: they work well for prolonged therapies, i.e. from a minimum of 3
months up to six months/one year. If they are used the patient will enter a condition of
"pharmacological menopause" for the period of therapy with all the resulting problems
- estroprogestinics and progestins: One type of estroprogestin is the birth control pill. In this case
the estrogen levels are lower, but always present in the therapy. Progestin is more suitable
because it is not associated with estrogen. As in the case of GnRH analogues, the therapy must be
continued for a certain period of time before changes are seen. It is therefore not possible that
from one day to the next the situation will change, you have to wait a few months.
- NSAIDs: they are administered for painful symptomatology
- antifibrinolytics: they are administered to patients with menorrhagia so important that they give
anemia.
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Vittorio Tuppo Rotunno

12/11/2019
Erika Balconetti
Gynaecology
Prof.
PID - PELVIC INFLAMMATORY DISEASE
PID is an inflammatory disease that affects some women who come into contact with some microorganism,
which ascendingly colonizes the uterus, tubes and, in some cases, the abdominal cavity.
Often women with a pathological picture of this type come to the emergency room with abdominal pain
perceived bilaterally in the lower quadrants or diffuse and, in addition to the differential diagnosis, it is
important to understand the severity of the problem, given the myriad of facets that these pictures present.
The most frequent localizations, beyond the banal vaginitis, are (in decreasing order of frequency):
- SALPINGI: the manifestations of which may be part of the classic salpingitis picture, which may be
hesitant in some more or less immediate secondary problems. One of the major ones is characterized
by tubal damage that can result in tubal sterility or tubal pregnancy, precisely because of the alteration
of the ciliated mucosa; other times tubal sterility can lead to an alteration in the geometry of the tuba,
compromising the normal peristaltic capacity which is one of the causes of tubal pregnancy.
- OVAIE: with the classic manifestations of ovaries.
- PARAMETRY, PERITONYPE: in this case the picture is that of a peritonitis with the involvement
also of other organs.
Infection of the epithelium leads to destruction of the epithelium, fibrosis and agglutination of the tubal folds,
especially in the cornual and fimbrial region. The greatest concern goes beyond the acute infection itself,
which can be resolved with an antibiotic or surgery: once acquired, the tubal damage lasts forever, involving
the woman's fertility expectations.
Etiology
In the past, the most important epidemiologically important microorganism was N. Gonorrhoeae, giving
infections in the urethra, cervix, which could then spread upwards to the tuba. This was a type of pathology
that was quite easily discovered because this type of purulent cervicitis led to the presence of a characteristic
bad smell together with a greenish exudate, which was the cause of apprehension on the part of the woman
who took her to seek medical advice.
Today, however, what is more widespread is a more clinically silent microorganism, but also more dangerous:
Chlamydia Trachomatis. Also this one, by ascending way, is able to colonize the tubes, destroying them, but
without giving a particular symptomatology.
Then there are also anaerobic bacteria such as E. Coli, Streptococcus, some Mycoplasms (not clinically severe
but extremely difficult to eradicate even with several cycles of different antibiotic therapies), Haemophilus,
Gardnerella, Clostridia and others. The main problem with these infections is detecting them, as a vaginal swab
is only performed outside the routine when there is a problem. This mainly concerns microorganisms that do
not give signs of themselves (see Chlamydia), while others such as Gardnerella give quite typical signs such as
the smell of rotten fish and a greyish patina, however, not very visible.
Epidemiology
Obviously, this type of problem mainly affects young women between 20 and 35 years of age, where not only
is there more sexual activity, but the higher number of partners is more important.
Acute and chronic salpingitis
Acute salpingitis can be catarrhal or interstitial, it can take the form of perisalpingitis or purulent salpingitis: an
inflammation can therefore give signs of if, but not all of them become purulent. The Sactosalpinge is what
usually hesitates an acute salpingitis, leaving a sign of itself, and it is nothing more than a salpin that stretches
out filling itself with exudate, blood or pus. In this case the sactosalpinge is visible on ultrasound because the
tuba stretches because it is full of material and therefore, not only do you have a symptomatology, but even a
good doctor may be able to see it on ultrasound with consequent greater diagnostic safety.
Chronic salpingitis, on the other hand, are those forms of salpingitis that have already hesitated in damage and
are therefore no longer solvable with an antibiotic. The damage can range from tubal deciliation, to
conglutination of the fimbriae and tubal ampulla and often even hesitate in a tubal occlusion, when not also or
in the formation of adhesions.
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In this image you can see how this tuba is stretched, practically attached to the uterine sacral ligament and
prolapsed into the Douglas' cord with loss of its normal geometry and shape. (image currently unavailable)
Obviously the occlusions can be of various entities (e.g. 20% after one recurrence or 80% after two recurrences
etc.) and this is relevant because it means not being able to have children in a natural way, even if it is good to
remember that even an acute salpingitis in the absence of tubal occlusion is enough, but with destruction of the
ciliate epithelium which implies the loss of normal functions by the tuba itself. So it is true that there is a 20%
probability of occlusion as a result of salpingitis, but it is also true that the probability of sterility in the absence
of occlusion is much higher although unknown. For example, in front of a couple who have been trying to have
children for two years and who in remote history show an acute salpingitis, but in the absence of evidence of
occlusion, it is necessary to question the integrity of the function of the tubes.
Risk factors
The risk factors for such an infection are various: IUD, concomitant or previous sexually transmitted
infections, sexual promiscuity with unprotected sex or a previous PID.
Even invasive medical maneuvers of a diagnostic type such as the maneuver itself or the dynamics involving
some tests that try to assess tubal patency can lead to a PID: every time you have to go to check the tubal
patency and then apply maneuvers such as sonohysterography, hysterosalpingography or Rueben (?) test by
laparoscopic means you must always give an antibiotic cover to the patients to protect them from some
microorganism that can eventually be brought inside the abdominal cavity by these procedures.
Oral hormonal contraception is not a risk factor for infections, let alone for cervical or cervical cancer, if
anything, patients who use it do not use condom to / from their partner increasing the chances of infection.
Clinic and diagnosis
Usually patients, when symptomatic and in the acute phase, present with various manifestations, including a
body temperature generally above 38 degrees.
Abdominal and gynecological signs are characterized by spasmodic, intense and bilateral pain localized to the
lower abdominal squares, which increases:
- with deep palpation;
- with the gynaecological examination at the same time as the mobilisation of the cervix or when the
pressure is applied more deeply: this is also called deep dyspareunia;
- Painfulness of the adjoining fields in the presence or absence of elastic tensile masses.
Urinary signs are similar - cystitis or discomfort during urination.
The lab tests that can certainly help in the diagnosis are:
- a blood panel with a formula that shows neutrophil leukocytosis;
- High PCR;
- ESR high;
- vaginal or non-vaginal swabs may or may not highlight certain bacteria, but it usually does;
sometimes it may be necessary to look for Chlamydia in blood or urine using PCR techniques.
- Finally, it is always necessary to do a pregnancy test on blood to a woman with abdominal pain,
precisely because one of the problems that afflict women with PID is precisely the extrauterine
pregnancy.
A negative laboratory test, however, does not exclude a PID and is therefore not sufficient to exclude it.
Of course ultrasound can always help, but clearly you can't see an inflamed tuba but at most a hydrosalpine,
pyosalpine, hemosalpine or any saccharged collections or a Douglas cable full of inflammatory material. An
endometrial sample can also be taken to assess that there is no endometritis, culdocentesis (a technique now
practically outdated) or a diagnostic laparoscopy, the latter always recommended in chronic and non-acute
situations, because in the latter case it is always necessary to wait and let the acute phenomenon cool down
with antibiotic therapy. Laparoscopy can simply be used to make a diagnosis, so it is always worth wondering
whether the diagnosis has in fact already been made clinically, to treat or operate, but in this case it makes
sense only after the acute phase of PID has been overcome.
Having made all these considerations, the diagnosis, in any case, is almost always eminently clinical, even if
due to the variability of symptoms it is often late, especially if the patient does not show up at the hospital,
where it is possible to make a series of tests that are unlikely to escape such an inflammatory/infectious
situation. You must also always keep in mind the differential diagnosis with pathologies such as: acute
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appendicitis, endometriosis, haemorrhagic corpus luteum, complications of an ovarian cyst (possible rupture or
torsion), extra uterine pregnancy.
Finally, it is worth mentioning a syndrome that leads a lot of women in hospital, who actually "have nothing"
and that is irritable bowel syndrome. Women suffer from irritable bowel syndrome and sometimes the pain is
frankly heavy, sometimes even incoercible with medication to the point of pushing them into PS and in any
case confronting the doctor with the need for a differential diagnosis with all that has been mentioned above.
Complications and natural history of the disease
Among the complications of salpingitis, the most important is certainly infertility. As a result of a PID a large
proportion of women have closed tubes or those that do not work and so tomorrow they may have difficulty
finding children. It also configures the possibility of:
- extra uterine pregnancies;
- liver syndrome, linked to pain in the right upper quadrant associated with perihepatitis;
- increased maternal and fetal mortality and morbidity in PID during pregnancy, that is why swabs are
taken during pregnancy and if particular microorganisms are discovered, antibiotic therapy should be
done;
- HIV positive patients may have even worse symptoms simply because they are defecated.
Thus, in the natural course of the disease, acute salpingitis can heal, especially if diagnosed early, following
antibiotic therapy with restitutio ad integrum or it can become chronic with probable loss of tubal function,
ovarian or Douglas tube abscess, rupture of the abscess with peritonitis, even to this syndrome characterized by
perihepatitis. Unfortunately, this type of pathology has a very strong tendency to recurrence, so much so that
many of these patients then present an adhesional involvement of the ovary with the uterus and tubes, therefore
sterility, and naturally increased risk of tubal pregnancy. Therefore, following a PID, not only are patients
invited to check themselves in the future due to possible infertility, but also and above all they are urged to
alert the gynaecologist in case of a positive pregnancy test because clearly a patient who has had a PID has a
much better chance of having a tubal pregnancy.
It is important to know that in most cases you cannot know if a patient has acquired tubal damage as a result of
a PID. When a gynaecologist sees in the remote pathological history a PID in a patient with a positive
pregnancy test, he must pay much more attention to the possibility of an extrauterine pregnancy and, at the
same time, if she wants children, he must warn her that she should try to have children a little earlier than she
wishes, the need to carry out a tubal check and that, if she is unable to have children, the etiology of sterility
will probably be due to the previous PID.
Question from a student: so a woman has never recovered until proven otherwise?
Teacher's answer: Practically yes, because the diagnostic examination that could or should be done is an
examination that would still give doubts in any case and secondly it is represented by surgery. All this would
mean that after healing the patient would have to undergo a laparoscopy and do a Rueben test: i.e. a
laparoscopy in which the normality of the uterus is checked, the presumed patency of the tubes, if they do not
appear congested and with an intact geometry, to get to the dynamic test in which methylene blue is passed
from a catheter inserted through the cervix to see if it passes or does not pass through the tubes. At this point,
however, at most we could only say that the tubes "seem" intact because maybe they are not detectable
adhesions, you can not see a marbled uterus, the tubes are readily open, not congested, etc.. but in any case
you should consider that it would not be enough, because you do not have a camera to look inside the tubes
and see if by chance the ciliate epithelium has not been damaged.
So a patient with a PID could perfectly have a problem-free pregnancy, just as she could have problems: this
only means that a previous PID is a warning sign in the case, for example, of a young woman looking for
children, while ovulating normally and maybe even with a husband with a normal ejaculate. Even in women
who are unable to have children, due to the absence of any kind of problem, and who do not report that they
have had a PID, because they may not know they have had it, a search for Chlamydia antibodies in the blood
can be carried out and if these are positive there is a 60% chance of having closed tubes.
Treatment and hospitalization
As far as the treatment is concerned, this is initially empirical because even in the suspicion of a PID it is
advisable to start an antibiotic treatment that in any case covers the patient. In case of confirmation, of course
the analgesic therapy applies, the partner can also be given a pharmacological treatment and if an IUD is
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present it should always be removed (even in case of suspected PID). In the case of an acute PID, if you think
that the lady can be well at home, you can think about prescribing therapy at home, while with regard to the
criteria of hospitalization, these can be outlined in:
- presence of a suspicious abscess;
- very high temperature, all the more so if he shows signs of septicemia like chills;
- particularly high leukocytosis;
- in case of non-response to antibiotic therapy at home;
- HIV positive patients must always be hospitalized;
- in the event of an ongoing pregnancy;
- presence of peritonitis;
- presence of IUD, in which case it should still be removed;
- dubious diagnosis;
Clearly each microorganism has its own specific antibiotic treatment, as long as you are aware of the
microorganism, while with regard to surgical treatment in laparoscopy this is to be avoided in the acute phase
and is aimed, in which case, to eliminate adhesions, drain abscesses, perform a salpingectomy in case of
pyosalpine.
CLIMATERY
The climacteric is that moment that lasts a few years before and a few years after the menopause when the
ovary no longer works well or dies completely. Just as there are premenopause, perimenopause,
postmenopause and senility there is also climaterium, a faded period ranging from ten years before menopause
to ten years after. Usually a woman goes through menopause from 45 to 55 years old, while the symptoms of
climacteric disease appear a few years before menopause. These represent that sequence of events that lead to
the condition of senescence, passing through various phases:
- premenopausal changes in endocrine structure and menstrual cycle that usually shortens;
- menopause, defined by the absence of menstruation for at least 12 consecutive months (in fact, after
the age of 50, 3 months are sufficient);
- perimenopause, that period ranging from 2 to 10 years before and up to 12 months after the last
menstruation;
- postmenopause: this latter period ranges from the certainty of menopause to senescence.
The climaterium manifests itself around the age of 50, but the range of normality goes from 45 to 51 years,
while if it starts earlier it is early menopause, otherwise late menopause. The fundamental cause is represented
by the end of the follicles, while the central causes revolve around the loss of the pulsatility of the GnRH that
stops due to the alteration of the LH/FSH ratio: the upset of these balances causes the lack of the GnRH
stimulus that cascade no longer stimulates all that phenomenon that leads to the functioning of the ovary. In
menopause there is therefore an upheaval of the gonadotropins' structure, detectable at sex hormone tests, and
characterized by a great serum elevation of FSH and LH caused by a decrease of functioning tissue of the
granulosa cells that produce estrogen, therefore a reduction of estrogen will also be observable due to the
absence of growing follicles and a functional deficit of the corpus luteum followed by a gradual zeroing of
progesterone; clinically at the beginning there are a series of anovulatory cycles until complete amenorrhea in
menopause. The increase in FSH, rather than a decrease in inhibin production, is due to a decrease in oestradiol
feedback, the levels of which are zero, while due to the decrease in dopaminergic activity there is an increase
in LH.
The 17-βestradiol, which is obviously the main hormone of the whole follicular phase, will have a production
not more ovarian, but only extraovarian: there will be some women who will have some estrogens still a little
visible, especially the fat or obese patients, this because the estrogen will no longer be produced by the ovary,
but only by the adipose tissue by conversion of the androgens into estrogens.
The extrone, on the other hand, is a little more abundant and is defined as the estrogen of the menopause and is
derived from the conversion of testosterone and androstenedione into adipose tissue.
Of course all this means that there will no longer be estrogen activity on target tissues such as skin, breast,
muscle tissue, bone tissue and others. Clearly the woman notices, also aesthetically, the change, just as she
notices the menstrual cycles that shorten around 45 years: if before, for example, this came every 28-30 days,
in this period of change comes every 25-26, we also notice the appearance of anovulatory cycles, long cycles
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but with a short luteal phase, a corpus luteum that does not work producing less progesterone, the appearance
of absolute or relative hyperestrogenism and obviously reduced fertility.
The ovary, however, also produces androgens (others are produced by the adrenal glands) which will undergo
a reduction in perimenopause, in particular DEA and DEAS, correlated with age which amounts to about 2%
per year. To this must be added a 40% reduction in SexOrmonBindingGlobulin levels from 4 years before
menopause and up to two years after menopause and a 20% reduction in testosterone immediately after
menopause and up to 80 years, after which there seems to be a very slight increase.
The reported changes in the cycle are represented by an increase or reduction, more often reduction, of
menstrual flow, although more than an increase in flow it would be better to talk about menorrhagia. All this to
say how about 90% of women before menopause experience irregularities.
During perimenopause, altered follicular development, increased LH levels, absence of ovulation despite high
estrogen levels, intermittent endometrial proliferation causing altered menstruation, resulting in abnormal
uterine bleeding can easily be observed. These bleedings of the perimenopausal period can be defined as
dysfunctional metrorrhagia or menorrhagia; the former occur 10 days after menstruation, the latter continue for
15-20 days after menstruation.
N.B. often the perimenopausal patient reports to the gynaecologist to have an abnormal loss in 20 weeks or to
have a menstruation that lasts for 15 days; these are cases of dysfunctional bleeding and are completely
consistent with perimenopause.
Differential diagnosis for perimenopause: anovulation, fibroids, adenomyosis, endometrial pathology, prolactin
and thyroid problems.
N.B. a fundamental element to make a diagnosis is age (e.g. if the patient has a symptomatology similar-
perimenopausal and is 20 years old, obviously it cannot be perimenopause).
PERIMENOPAUSE SYMPTOMS
 Vasomotor symptoms
 Psychic symptoms
 Local and systemic symptoms related to estrogen deficiency
HOT FLUSH, hot flush: intense sensation of heat that suddenly rises in the chest and spreads to the neck, face
and sometimes the whole body; it lasts a few minutes and often manifests itself with sweating, palpitation and
tachycardia. It is connected to hypoestrogenism, which by increasing norepinephrine and reducing dopamine,
causes the lowering of the central thermostat set point with its vasomotor reaction (vasodilation and sweating),
in an attempt to lower the body temperature. The hot flush usually lasts a couple of years.
MODIFICATION OF THE HUMOR TONE: many women have a change of mood in the perimenstrual
period; a percentage will have it also in the perimenopausal and menopausal period. Psychic symptoms,
typically anxiety and depression, have a meaning that goes beyond hormonal change, since they can be due to
physical changes the perimenopausal woman experiences or changes in her life (e.g. the perimenopausal
period usually corresponds to the time when her children leave home); the mood tone can also be particularly
affected by sleep deprivation due to flushing and night sweats.
N.B. Usually a woman in menopause complains of vasomotor and psychic symptoms, but in reality it is the
symptoms that are not perceived that give more concern.
SYSTEMIC EFFECTS OF ESTROGEN DEFICIENCY
 Increased risk of cardiovascular disease (e.g. hypertension)
The protective effect of oestrogen, which inhibits the proliferation of smooth muscle cells and vessel
remodeling, exposing women to cardiovascular problems, disappears; in fact, if the risk of coronary
heart disease is lower for women in fertile age than for men, around the age of 65 the risk for women
and men evens out.
 Osteoporosis, a multifactorial systemic disease characterized by a reduction in bone mass per unit
volume. There is an alteration of the bone microstructure, so that the bone becomes less trabecular,
emptier and weaker, increasing the risk of fracture. In postmenopausal osteoporosis the most frequent
fractures are at the vertebral site, at the distal end of the forearm and femur. For a woman the risk of
developing a fracture during her life is 40-50%.
 Skin aging
 Increased risk of degenerative diseases (e.g. Alzheimer's disease)
 Altered lipid balance
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 Altered glycidic metabolism

In the perimenopausal period the woman tends to gain weight because the basal metabolism
decreases; in addition a wrong lifestyle, bad eating habits and lack of exercise worsen the situation.
 Increase in total cholesterol
 LDL increase
 HDL reduction
 Reduced pancreatic insulin secretion and increased peripheral insulin resistance
LOCAL EFFECTS OF ESTROGEN DEFICIENCY
Estrogen deficiency, resulting in decreased collagen, epithelial thinning, modification of bacterial flora and
reduced lubrication, causes urinary tract atrophy, vaginal atrophy and susceptibility to infections with recurrent
vaginitis and cystitis.
Urogenital symptoms: vulvovaginal atrophy, dryness in 27-40% of cases, dyspareunia (pain during
intercourse) in 9-25% of cases, recurrent vaginitis in 9-23% of cases, burning in 9-23% of cases, vulvar
itching, low urinary tract atrophy, frequency of urination, nocturia, recurrent infections.
One of the most interesting urogenital symptoms from a surgical point of view is prolapse: the lack of estrogen
could cause the vaginal walls to descend associated with the descent of the uterus due to the sagging of the
supporting tissues of the perineum; in other words, the tissues supporting the pelvic floor slowly sag and the
uterus slides inside the vagina, protruding outside the vulva.
Symptoms of prolapse: lumbosacral pain and feeling of heaviness, possible genital leakage from the vulvar
rhyme in orthostasis, urinary symptoms (pollakiuria and incontinence) due to dislocation of the bladder being
brought down from the uterus and rectal symptoms; there is solidarity between the pelvic organs, so that the
uterovaginal prolapse is associated with descent of bladder and rectum, leading to cystocele and rectocele.
There are three degrees of uterovaginal prolapse:
 uterovaginal prolapse of 1st: uterus descends and stops in vagina
 uterovaginal prolapse of 2nd: the uterus descends and arrives at the hymen.
 uterovaginal prolapse 3°: the uterus descends until the cervix comes out of the vagina.
DIAGNOSIS OF MENOPAUSE
 Age
 Anamnesis
 Clinical: the climatic pathology always manifests itself with hot flushes, which are accompanied by
palpitation, insomnia and reduced concentration, altering the quality of life; if the patient is ill she
must be helped. Asthenia and vaginal dryness, although they occur in most women, do not always
require therapy, which is only required in the presence of regular sexual activity. Urinary disorders are
fatal and should therefore be detected and treated as soon as possible. The pain in the cervical, dorsal
and lumbar area is related to osteoporosis.
 Hematochemical tests: in the menopausal period it is advisable to perform an evaluation of FSH
(increases by about ten times), estradiol (resets to zero; the only estrogen of the menopause is
extrone), LH (increases), progesterone (decreases; androgens gradually reduce and reduce the effect of
testosterone).
 Ultrasound: trans-vaginal ultrasound evaluates the thickness of the endometrial rhyme which must be
thin in the menopausal period.
It is essential to frame a woman in menopause at an early stage, so as to be able to assess the presence of risk
factors related to menopause (cardiovascular diseases, osteoporosis, tumor pathology, incontinence) and
establish the therapy.
The osteoporotic risk is person-dependent, being linked to genetics and lifestyle: women who smoke, have bad
eating habits and do not exercise are more likely to develop osteoporosis. Menopausal women undergo bone
densitometry to assess bone quality and determine the amount of calcium to be taken.
The risk of cancer can be countered by screening procedures by subjecting a woman over 50 to a mammogram
every year for the prevention of breast cancer, by performing fecal occult blood tests every two years for the
prevention of colorectal neoplasia and by performing a pap test every 2-3 years for the prevention of cervical
cancer.
Question from a student: is it true that the pap test can be suspended after a certain age?
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Answer: The pap test is performed to assess the presence of cells altered due to HPV; there are about 200
types, including 50 sexual isotypes, some of which are oncogenic. So it would be worth it in a 40-year-old
woman who is not sexually active (cervical cancer is not necessarily 100% caused by sexual HPV), but it
could actually be avoided in an 80-year-old woman for example.
HSC hysteroscopy is only performed in the presence of AUB, i.e. abnormal bleeding. In menopause the ovary
does not work and you can't have menstruation; if there should be blood loss you should understand where it
came from.
The assessment of urinary incontinence goes through a series of urodynamic examinations to determine the
cause and severity, since some women may experience difficulty in emptying their bladder and must therefore
undergo surgery, eliminating the uterus and repositioning the bladder, so as to allow normal urination and a
normal life: flowometry (evaluates urinary flow based on the rate at which urine is expelled from the urethra),
cystometry (records bladder pressure by checking the detrusor muscle), sphincterometry (measures pressure in
the urethra at rest and under stress) and instantaneous mintional sphincterometry (measures bladder, urethral,
intra-abdominal and sphincter pressure when the bladder is full). These tests allow to understand if the
incontinence is due to the detrusor or the urethra, thus deciding the type of intervention.
CLIMACTERIC THERAPY
Until the 1990s, many women resorted to menopausal therapy, although many did not need it because the
lifestyle was quite calm, because it was well publicized. In the last twenty years, women's lifestyles have
changed and requests for estroprogestin therapy have increased, despite the fear of cancer.
Menopause is not an illness, but a fundamental stage in a woman's life, during which if you are sick you can
feel better. Menopausal therapy, in fact, does not necessarily have to be submitted to every woman; however,
every woman in menopause should act on some aspects (reducing stress, changing dietary style by increasing
the calcium dose and reducing calories, smoking cessation, adequate physical activity), in order to avoid a
rapid decline and drastically lower the quality of life.
HRT menopausal therapy consists of a hormone treatment based primarily on hormones once produced by the
ovary, estrogen and progesterone, allowing the woman to stay young. Hormones can be administered by os,
transdermal, intramuscular, vaginal or nasal route. In pharmacies there are ready-made formulas, but it is still
possible to create combinations "playing with fantasy": e.g. giving estrogen x to dosage y per os, adding
progestin x to dosage y as a patch. Hormone therapy can be sequential cyclic, continuous cyclic, continuous
combined or continuous with estrogen only.
Sequential cyclic therapy is indicated if the woman asks to menstruate; it is a therapy based on estrogen for 21
days and progesterone from the 10th to the 21st day, determining the hormonal deprivation that causes
endometrial desfoliation and then menstruation, at the end of which the cycle is repeated (like the pill).
Continuous cyclic therapy is indicated if the woman does not want menstruation; estrogen is taken every day
and progesterone only in the second phase.
Continuous combined therapy is based on the simultaneous, non-staggered intake of estrogen and
progesterone, blocking menstruation.
Continuous therapy with only estrogen is a risky variant and should only be applied in women who have had
their breasts and uterus removed.
When is menopausal therapy indicated? In symptomatic women, women at risk of osteoporosis and/or
cardiovascular disease and women in early menopause or surgery.
Among the contraindications are the classic contraindications of estroprogestinic therapies (such as the pill)
and related contraindications to be evaluated with the patient.
To conclude, the professor mentions the WHI study carried out in the 1990s, on a sample of 16,000 women
aged 50-79 years, some of whom were taking a placebo while others a combination of natural estrogen and
progestin pills. The study, which should have lasted eight years, was discontinued because a relatively higher
relative risk of breast cancer (8 more cases per year out of 10,000 women), stroke and pulmonary embolism
had been reported in women undergoing treatment, but without disclosing the benefits of the treatment (e.g. 5
cases less the year of hip fracture, 6 cases less the year of colon cancer). Therefore, for fear of developing the
tumor more easily, hormone therapy has drastically decreased in the years 2000-2010; only in recent years is it
re-flowering.
Replacement therapy is contraindicated in women with previous breast cancer (being at high risk) and in
women with hysterectomized endometrial cancer; since most recurrent endometrial cancer problems occur
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within two years of initial diagnosis, therapy should not be started before two years. To date, epithelial ovarian
cancer is not a contraindication to therapy. Beyond the replacement therapy, it is possible to use specific drugs
for vasomotor disorders or specific drugs for osteoporosis or drugs that act selectively on estrogen receptors
giving significant results in terms of symptoms, positive effects on calcium metabolism and bone density,
improvement of the lipid profile with protective effect on cardiovascular diseases, reduction in the incidence of
breast cancer, but without giving effect on vasomotor phenomena and endometrial proliferation.
CONCLUSIONS
Women who have serious problems at the beginning of menopause and who suffer from serious problems that
worsen their quality of life must start substitution therapy. Replacement therapy will produce long-term
benefits on bone mass. Prolonged treatment can increase the risk of breast cancer but reduce the risk of colon
cancer. Short-term therapy within five years is probably the best therapy you can do. In the absence of major
menopausal disorders, women should evaluate the costs and benefits with the professional. In women with
premature menopause (35-40 years) spontaneously or caused by the removal of the ovaries, the therapy does
not involve any additional risk and is strongly recommended. Taking therapy should not lead to neglect of the
right lifestyle.
STERILITY AND PMA TECHNIQUES
This is a very popular topic at the moment. According to data published on the website of the Italian Society of
Gynaecology and Obstetrics, 25% of Italian couples need to see a doctor who deals with infertility. Bearing in
mind that in Italy about 500,000 children are born, of which 100,000 from non-EU countries and 400,000
from Italian couples, almost 100,000 couples (25% of 400,000 Italian couples, a very high number) may have
needed a doctor to take care of reproduction.
DEFINITIONS
FERTILITY: ability of living beings to reproduce with conservation of the characteristics of the species.
STERILITY: inability to conceive after at least 12 months of unprotected sexual intercourse (reduced to 6
months in older subjects).
- PRIMARY STERILITY: absence of previous conception.
- SECONDARY STERILITY: established after a period of documented fertility.
INFERTILITY: inability to complete a pregnancy.
In Italian the terms "fertility" and "sterility" indicate different concepts while in English the terms "fertility"
and "sterility" indicate the same
thing.
In the human species the average

fertility rate is not very high: only
25% of couples who have regular
unprotected relationships get
pregnant during the first month and
it takes about 1 year for pregnancy
to occur in 90% of cases.
EPIDEMIOLOGY
In the Western world 15% of couples have an infertility problem. The incidence is increasing because:
- ↑ ↑ average age at which pregnancy is sought;
- ↑ incidence of sexually transmitted diseases;
- ↑ incidence of OTA (oligoteratoastenozoospermia).
CAUSES OF STERILITY
- Male factors (35%);
- Female factors (40%);
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- Immunological and torque factors (10%);

- Idiopathic sterility (no diagnosis at the end of the diagnostic path) (15%). However, this does not
mean that couples will not be able to have children naturally. It is linked to our inability to make a
diagnosis, so it is likely that in the next few years the percentage will tend to decrease.
Female causes of infertility

- Endocrine causes (40%):
o Anovulatorship (difficulty or inability to ovulate):
 by hypothalamic cause (of organic nature - neoplasms, malformations, inflammations -
functional - anorexia nervosa, post-pillar amenorrhea);
 by pituitary cause (mainly adenomas, hyperPRL, rarely Sheean's sdr.);
 by ovarian cause:
 polycystic ovary syndrome (PCOS);
 Early Ovarian Failure (POF);
 genetic anomalies (Turner's sdr. and mosaicisms);
 results of chemo- and radiotherapy (therapies that may have decreased the woman's
follicular heritage);
o Altered corpus luteum function;
o Extraovarian endocrine alterations (hyperPRL, hyperA - hyperandrogenisms -, dysthyroidisms,
which may affect the proper functioning of the hypothalamic-pituitary-gonadal axis);
- Tubal-pelvic causes (35%): these are mechanical/hydraulic causes that prevent the spermatozoon
from meeting the oocyte. Etiology: prev. due to inflammatory processes (PID, ascending infections by
N.Gonorrheae, C. Trachomatis - the most frequent -, TB); endometriosis (generalized inflammatory
condition not secondary to infectious events related to tubal geometry alterations); previous GEU
(extrauterine pregnancy); scarring results of abdominopelvic surgery.
o Structural alterations of the salpingi: obliterations (prev. post-inflammatory), stenosis,
terminal phimosis, fibrosis of the muscle cassock, alterations of the ciliated epithelium,
agenesis;
o Functional alterations of the salpingi (therefore the tubes are pervie): abnormal peristalsis,
spasms;
- Uterine causes (10%):

o Endometrial polyps;
o Myomas (submucosis - particularly G0 and G1 protrude into the uterine cavity -, intramural);
(polyps and myomas are the most frequent conditions)
o Malformations (septa, bicorne uterus, etc.);
o Sinechie (adhesions);
The picture opposite shows possible uterine

malformations, conditions that can
sometimes allow the woman to have children
if the uterine cavity in which the embryo will
nest is sufficiently complimentary to a
pregnancy.
A. Didelphus uterus with double vagina
(usually one vagina is larger than the
other, as is the corresponding uterus). It
is not possible to perform a metroplasty
in order to merge the two uterine
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cavities, it is only possible to study the condition and hope that one of the two uteruses is large
enough to allow a pregnancy;
B. Arched uterus: normal uterus in the presence of an accentuated concavity at the bottom. If this
concavity is determined by muscle, no action is taken, otherwise if it is fibrous, a metroplasty can
be performed in order to make the cavity a little wider;
C. Bicorne uterus: it is important to distinguish it from the didelphic uterus (on ultrasound it may
look the same, but the bicorne uterus has a unique vagina). There is a double neck and usually
one uterus is larger than the other. The middle fabric can be worked to create a little more space,
but the two horns will remain (it is not possible to fuse them together). The bicornuate uterus
should also be distinguished from the septated uterus on ultrasound and hysteroscopic
examination because the median tissue in the bicornuate uterus is muscular, while in the septated
uterus it is fibrous and can therefore be removed (if the muscular tissue of the bicornuate uterus
were to begin to be removed, in addition to obtaining significant bleeding, it would end up in the
abdominal cavity);
D. Bicorne unicervical uterus (kidnapped horn) - the professor has never seen one;
E. Cervical atresia - the professor has never seen one;
F. Vaginal atresia (found in some syndromes, such as Mores syndrome - I don't know if this is
correct - but not at infectious events).
G. From Pathological Anatomy: Septic uterus: the uterine lumen is divided into two hemiuteri by the
presence of a septum, which can extend from the bottom to the cervix (complete) or be shorter
and not reach the internal uterine orifice (incomplete); sometimes the septum can also extend in
the context of the vaginal lumen, also dividing it into two hemiuteri;
H. T-shaped uterus: malformation characterized by a narrow uterine lumen, which takes the form of
a T, due to the increased thickness of the side walls; it is due to the intake of diethylstilbestrol, an
estrogenic drug no longer used (it was used to prevent the threat of abortion from the 1940s to
the 1960s)].
- Cervical causes (5-10%):

o Quantitative alterations of cervical mucus for:
 Estrogenic stimulation deficit;
 Scarcity of the secrete epithelium (conization, DTC).
This leads to vaginal pH acidification and reduced sperm capacity.
o Qualitative alterations of cervical mucus for:

 Cervicitis;
 Estrogenic deficit;
 Anti-sperm antibodies;
In the periovulatory phase, at the moment of the oestrogenic peak, the mucus is very stringy and
allows the spermatozoa to pass well, whilst when there is no oestrogenic peak the cervical glands
produce less mucus and more viscous which makes the passage of the spermatozoa difficult.
- Vaginal causes (5%):

o Malformations (sepsis, stenosis);
o Vaginitis (PH alterations);
o Vaginism
So in most cases the woman's inability to have children is due to endocrine or tubal-pelvic causes.
PCO SYNDROME (PCOS)
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When it comes to anovulatorship or endocrinological disovulatorship, it is polycystic ovary syndrome that is

the main one. It is a syndrome that can also be recognized from a phenotypical point of view (women with an
abdominal and visceral fat disposition, like men) and a hormonal disposition characterized by:
- ↑ LH/FSH ratio (ratio no more than 1:1 but 2:1);
- ↓ ↓;
- ↑ Free testosterone (due to decreased liver synthesis of SHBG);
- ↑ DHEAS (of adrenal origin);
- ↑ Extrone (of adrenal origin);
- ↓ ↓.
All this creates alterations in the feedback mechanisms of the hypothalamic-pituitary-gonadal axis and
therefore chronic anovulatorship.
ALTERATIONS TO ENDOCRINE ACTIVITY IN THE CORPUS LUTEUM

INSUFFICIENCY OF THE LUTEUM BODY: due to altered follicular maturation and/or inadequate peak LH.
It determines insufficient production of Progesterone (in the second half of the cycle, after ovulation), which
hinders the nesting and development of the embryo due to failure to modify the endometrium.
LUF SYNDROME: particular syndrome, often unrecognized, in which ovulation does not occur, as well as the
release of the oocyte; the unbroken follicle undergoes luteinization and therefore the plasma levels of
Progesterone in the second half of the cycle are normal.
In this syndrome, therefore, the woman believes that she is ovulating (and the doctor believes that the woman
is ovulating) because she is menstruating, on ultrasound a growing follicle is visible and Progesterone levels in
the second phase of the cycle are normal.
HYPERPROLACTINEMIA
PRL is a hormone involved in:
- ovarian steroidogenesis (determines reduction of GnRH secretion);
- follicular maturation;
- formation and maintenance of the corpus luteum.
HYPERPROLACTINEMY (from functional/organic cause) leads to ANOVULATORY +/- AMENORREA.
Depending on the level of PRL you have different possibilities:

[PRL] between 21-29.9 µg/L → menstrual disorders in 30% of cases;
PRL] between 30-49.9 µg/L → anovulatory cycles in 67.5% cases;
PRL] between 50-99.9 µg/L → anovulatory cycles in 90% cases;
[PRL] > 100 µg/L → anovulator cycles in 100% cases.
Depending on the level, a medical or surgical approach should be considered (in case of organic problems).
ALTERATIONS IN THYROID FUNCTION

- HYPOTIROIDISM (thyroid function deficit, a fairly frequent condition in women of childbearing
age) leads to an increase in FSH and PRL and therefore to anovulatorship due to altered feedback
mechanisms;
- HYPERTIROIDISM (thyroid hyperfunctionality) leads to an increase in circulating estrogens and
therefore to anovulatorship (always due to an alteration of the feedback mechanisms; in this case the
excess of estrogens makes FSH unable to induce the maturation of the follicles and the selection of a
dominant follicle).
In both cases there is therefore anovulatorship, perhaps not every month (disovulatorship).
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ENDOCRINE CAUSES: DIAGNOSTIC INVESTIGATIONS

Purpose: to ascertain the presence of ovulation and an adequate hormonal climate.
Lab investigation:
- Hormone dosages on day 3 of the menstrual cycle to assess FSH, LH, E2 (estradiol), P (progesterone),
T (testosterone) free, SHBG, adrenal androgens, PRL and TSH, T3 and T4;
- Serious plasma dosages of estradiol, progesterone, LH to identify the ovulatory peak of LH;
- Plasma progesterone dosing in the luteal phase to ensure proper functioning of the corpus luteum.
In this way you get a complete evaluation (during the whole period) of the woman's cycle.
Alternative methods to (less sensitive) hormone assays - the prof defines them as additional investigations
after those described above:
- Assessment of cyclical, quanti- and qualitative changes in cervical mucus;
- Urinary ovulation test (for evaluation of LH peak);
- Measurement of basal temperature (↑ Body T ≥ 0.3°C after ovulation for
the production of progesterone, hyperthermic hormone).
Instrumental investigation:
- transvaginal pelvic ultrasound:
o morphological evaluation of uterus and adnexa;
o monitoring the presence, number and development of ovarian
follicles and corpus luteum;
o evaluation of endometrial changes during the menstrual cycle
(the appropriate thickness for lutein implantation is between 8-
13 mm);
- endometrial biopsy: allows to evaluate ovarian function and to diagnose

ovulation.
DIAGNOSTIC INVESTIGATIONS FOR FEMALE STERILITY

- OBJECTIVE EXAMINATION;
- EMAT-CHEMICAL EXAMINATIONS (ovulation, PRL, TSH);
- INSTRUMENTAL INVESTIGATION:
o Pelvic ultrasound;
o Hysterosalpingography/Sonohysterography: evaluation of anomalies in the uterine cavity and
tubal patency;
o Hysteroscopy: assessment of cervical canal, uterine cavity and tubal hosts;
o Laparoscopy;
- LABORATORY INVESTIGATION:
o Vaginal and cervical swabs;
o Muco-cervical compatibility test (today much less is used; it consists of taking a mucus
sample during the ovulatory period and placing it inside the spermatozoa: the ability of the
spermatozoa to migrate from one point to another is evaluated. The outcome is influenced by
the characteristics of mucus, spermatozoa or even the presence of anti-sperm Abs).
QUESTION: Are anti-sperm Abs directed against the sperm of a specific partner or against sperm in general,
regardless of the partner?
ANSWER: There are women with Abs of both types. In particular, it is reported in the literature that having
sex with a partner (who ejaculates in the vagina) for more than 10 years eventually leads to the production of
specific Abs against his spermatozoa. So having long engagements and then trying to have children seems to
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be counterproductive: e.g. if two boys get engaged at 15, stay together for 15 years and then try to have
children, it will be more difficult for them than a couple who get together a few months earlier.
In 2010-2011 the professor carried out a very interesting study (first in the world) in which he evaluated how
H. Pylori's anti-flagell Abs can cross-react with the scourge of spermatozoa; therefore in his study, treating
women with omeprazole, the percentage of pregnancies was higher.
An examination to be carried out to assess tubal patency is hysterosalpingography, which today is less used.
It was used a lot until 20 years ago; radiologists used to introduce mdc into the uterus by means of a metal
catheterine and then perform an Rx (if the salpingi are pervie the mdc passes inside and you can see them on
the Rx). At the end of the 90's, together with other physicians, the professor carried out a study on the
sonoisterosalpingography: physiological solution is introduced into the uterus and a 2D ultrasound is carried
out to assess whether the liquid also passes inside the tubes. With the evolution of the ultrasound scanner and
the introduction of the echocolordoppler, it has been possible to obtain clearer images.
With hysteroscopy, the uterine cavity is assessed directly.
Asherman's uterus is a uterus completely closed by synaecia.
FEMALE INFERTILITY THERAPY

(variable depending on aetiology)
 Pharmacological induction of ovulation;
 Uterine pathology surgical correction;
 Tubal pathology surgical +/- conservative correction, IVF (in vitro fertilization embrio transfert). In
the case of salpingoplasty (surgical correction of tubal pathology), the correction of epithelial defects
is practically impossible, so these patients will necessarily have to perform IVF;
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 Cervical pathology antibiotic/estrogenic therapy. Often, women with cervical disorders can benefit
from IUI (intrauterine insemination) in order to become pregnant, as sperm are deposited beyond the
cervix;
 Endometriosis medical therapy or surgical therapy and, in case of failure of both, IVF.
MALE CAUSES OF INFERTILITY

There are 3 categories:
 Hormonal problems: altered steroidogenesis due to hypothalamic, pituitary or testicular causes
(secretory sterility);
 Testicular problems: altered sperm production and/or maturation (secretory sterility);
 Post-testicular problems: in this case, the testicle is normal, the hypothalamic-pituitary axis is
functional, but sperm transport is altered due to congenital, inflammatory, traumatic/surgical causes
(excretory sterility).
Which, between secretory and excretory sterility is less serious? In the field of secretories, it is better to have a
hypothalamic/pituitary deficit (the testicular is the worst) because, with the administration of gonadotropins, it
is possible to restore a physiological picture; in the case of excretory sterility, the spermatozoa are normally
produced, so it will always be possible to take them; for example, they can be taken with needle aspiration in
the epididymis or, if they are not found in the epididymis, they can be sought directly in the testis. Clearly,
sperm taken in this way cannot be used for natural fertilisation, it will be necessary to carry out in vitro
fertilisation, through the so-called "Intracytoplasmic sperm injection" (ICSI). To do this, it is necessary to use a
needle eight times thinner than a hair through which the sperm are injected into the oocyte cytoplasm.
Secretory sterility of testicular origin requires a sperm donor for conception.
HORMONAL CAUSES
 Primary hypogonadism, in which the testicles do not produce testosterone (hypergonadotropic
hypogonadism). This is the worst you can have (among the hormonal causes) because it is as if man is
in "menopause". Hypogonadism determines the presence of small testicles, lack of testosterone
production and an increase in gonadotropins. The causes of hypergonadotropic hypogonadism can be
congenital or acquired. Congenital diseases include genetic or chromosomal diseases (Klinefelter's
sdr.), while those acquired include trauma, surgery, cancer, radio and chemotherapy;
 Secondary hypogonadism, in which the pituitary gland does not produce FSH and LH
hypogonadotropic hypogonadism. In this case, with a drug therapy (gonadotropins), the situation is
resolved. In fact, the condition is characterized by a healthy testicle that does not produce sperm due
to lack of gonadotropins (so we will have low gonadotropins and reduced testosterone);
 Tertiary hypogonadism, in which the hypothalamus does not produce GnRh hypogonadotropic
hypogonadism. Also in this case the situation is resolved by drug therapy (administration of GnRH).
 Hyperprolactinemia, infrequent in men and very frequent in women. In both sexes the most frequent
cause of hyperprolactinemia is the presence of a pituitary adenoma. This leads to an alteration of the
hypothalamic-pituitary axis with hypogonadism, impotence, oligospermia, galactorrhea, reduced
libido, headache, hemianopsia bitemporal. These are patients who may not even notice the problem
but, on objective examination, observing the presence of gynecomastia and hypogonadism in
association with reduced libido, one must think not only of the presence of a genetic syndrome, but
above all of hyperprolactinemia.
Hyperprolactinemia could also be related to stress but it is not such a frequent cause (although a large
incidence of males suffering from hyperprolactinemia was observed in concentration camps during
World War II. These men, despite their malnutrition thinness, had gynecomastia). Currently, however,
the most frequent cause is pituitary adenoma;
 Thyroid dysfunction, although, fortunately, it is rare in humans to observe thyroid dysfunction at a
young age:
o Hyperthyroidism: can be associated with pituitary gland malfunction and therefore cause
alterations in spermatogenesis;
o hypothyroidism: often associated with hyperPRL.
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TESTICULAR CAUSES
 Cryptorchidism factors we discover with the history

 Testicular torsion
 Varicocele, you investigate if there is no history with a visit looking if the pampiniform plexus is ectasic
or if it has pain. The varicocele is characterized by valve bleeding with compromised venous return
system and stasis which locally increases the temperature. It ultimately causes dysfunctions in sperm
production due to malfunctioning leydig cells and sertoli.
 Inflammations / infections
 Toxic substances and heat. The heat is extremely harmful to fertility as is clearly demonstrated by the
sterility of almost all the drivers of the old coal trains who spent the day in front of the coal furnace
which was right at testicular height. Testicles are supposed to "stay cool." They should not be exposed
to excessive or prolonged heat sources; moreover, tight jeans are not suitable for long walks because
they cause friction and overheating.
 Antisperm antibodies
POST-TESTICULAR CAUSES
Post-testicular problems can be:
o obstruction of the excretory tract, given by microorganisms
(always the usual)
o erection disorders for:
 neurological problems
 genital trauma
 endocrine causes
 medicines (antihypertensives and antidepressants
especially)
 abuse of drugs and alcohol: even in young people they
can cause the production of asthenic spermtozoa, which
they are unable to produce even though they do not
seem to influence their numbers (from studies made by the professor) (studies in general
seem to indicate that chronic consumption is much more impactful than occasional
consumption and that the influence is more qualitative than quantitative n.d.s.).
o Ejaculation disorders:
 Premature ejaculation
 Delayed ejaculation
 Retrograde ejaculation is caused by previous surgery or anatomical malformation and causes
bladder ejaculation. It is resolved by first ejaculating and then urinating the patient and then
taking the sperm for in vitro fertilization from the urine.
 Anejaculation can have psychological or organic causes or spinal trauma, but it makes no
difference since in vitro fertilization can always be done as long as the patient produces the
sperm.
The professor does not deal with the latter disorders, but surely medically assisted procreation will find a
solution if the others fail.
Anamnesis and objective examination
must be done. A particular sign of
alarm is a small testicular volume
that is measured with the orchimeter (a
sort of caliber to compare the size of
the patient with normal ones), very
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useful because in general you do not know if your testicles are average. The following controls are the
spermiogram and the hormone dosage.
The spermiogram is generally sufficient to give an idea whether the subject is able to procreate or not. Evaluate
macroscopic and microscopic parameters both important.
We'll see:
 rheological characteristics i.e. appearance (including colour and odour), viscosity and fluidification
 volume that is normal between 2 and 6 mL (even too large a volume indicates a problem, usually
infimmatory)
 pH
 nemaspermic concentration or the number of sperm per mL
 total number of spermatozoa
 percentage of motility
differentiated by type; in fact
there are 3 types of
spermatozoa with straight
mobility (they go straight and
fast), those with S-shaped
motion (they go a little to the
right and a little to the left)
and those that tend to turn on
themselves.
 non nemaspermic cellular
component or any other type
of cell that ends up in the
sperm (leukocytes, epithelial
cells, blood cells, ...) that are
used to understand if the
ejaculate is normal
[the teacher says to learn the parameters of the spermiogram in the table]
Terms to know:
1. normozoospermia
2. oligozoospermia =
few spermatozoa
3. asthenozoospermia
= asthenic
spermatozoa
4. teratozoospermia =
non-normal
spermatozoa
5. oligo-asthene-
terato-zoospermia
6. cryptozoospermia =
spermatozoa not
detected on the
spermiogram but
found after centrifugation
7. azoospermia = there are no sperm even after centrifugation
8. aspermia = absence of ejaculate; i.e. absence of both spermatozoa and seminal plasma (normally
produced by the pude urethral bulb gland, seminal vesicles and prostate)
MALE STERILITY THERAPY
Infectious and inflammatory diseases antibiotics
Gonadotropin hypogonadism (FSH, hCG)
Anatomical alterations (cryochidism, varicocele) surgical correction
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Azoospermia search for sperm in the testicle and epididymis (biopsy) and then if intracytoplasmic sperm
injection is found (ICSI)
IDIOPATHIC STERILITY
All those couples in which a cause is not found through both Level I and Level II investigations. What has to
be considered is that age is a cause in itself! Children don't come naturally when you're old. Women over 46
are unable to have pregnancies except for rare exceptions. Famous peronagos who have children far advanced
in age resort to egg donation.
CLINICAL APPROACH TO THE INFERTILE COUPLE
The wait is justified: trying to have a child naturally for a year is normal. Since the woman is 35 years old,
however, it is starting to be too much and in fact the WHO guidelines recommend to start checking after 6
months. On the one hand it is alarmism as a suggestion, on the other hand it protects us from the drastic drop in
fertility that occurs after the age of 35. Young couples however tend to come after years of trying and this may
not be a problem, while 40-year-old couples should consult their doctor as soon as possible at least for basic
tests such as the dosage of gonadotropins especially the anti-Müllerian hormone (in 3rd day) which tells us
how many oocytes are left. This is because the woman should know if from a hormonal point of view
everything is still okay and therefore she still has a chance or if the menopause is very close. This serves to
orient both the couple and the doctor who must advise them properly.
At the moment most in vitro fertilizations are autologous (i.e. done with their own eggs), but the number of
heterologues is increasing exponentially because there are many couples who want a late baby.
What's the procedure? Step by step. First with tips to find the right day for ovulation, then intrauterine
inseminations can be done and afterwards more aggressive therapies may be necessary. Very often you get to
in vitro insemination overcoming problems of which you were not aware (maybe solvable), but so much the
couple manages to have the baby and is happy.
ASSISTED REPRODUCTION TECHNIQUES
LEVEL: in vivo techniques
It includes any help given by doctors that leads to the meeting of the oocyte and spermatozoon in the tuba so
both scheduled sexual intercourse and intrauterine inseminations that mimic a natural intercourse, but the
semen is not ejaculated in the vagina but is inserted into the cervix.
II LEVEL: in vitro techniques
When the egg and sperm meet in the lab.
INTRAUTERINE INSEMINATION
It consists of introducing the semen into the uterine cavity by means of a special catheter after washing and
capacitation of the ejaculate. In the early days of this technique, the semen was shot into the uterus directly
carrying the bacteria and prostaglandins that caused the woman excruciating pain because they stimulate the
muscles. Only then did it become clear that the ejaculate had to be not only filtered and treated, but also
capable because otherwise it was not able to fertilize. The aim is to place a concentration of motile sperm, the
best, in the uterine cavity during ovulation. The treatment of the ejaculate is also used to select the best
spermatozoa (those that have gone up the centrifuge three times) and at that point they are introduced instead
of 500 million even one and a half million (minimum).
The directions are:
 mild oligo-astenozoospermia, as they particularly benefit from a treatment that selects and
concentrates healthy spermatozoa
 dysovulatory sterility, because you allow the woman to produce the follicle and have ovulation and
then do the insemination on the right day raising the chances very high
 vaginal sterility
 cervical sterility, in which the woman may be producing antisperm antibodies
 unexplained sterility
It is done for a maximum of 6 cycles in general.
With the speculum you enter the vagina, enlarge it, observe it and then find the neck of the uterus to staple it
and then pass the catheter through the external and then internal uterine orifice and finally deposit the semen at
the bottom of the uterus where it will begin to move and look for the oocyte.
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You can do it up:

 natural cycle: you study it with ultrasound
and blood tests and find the right day.
 stimulated cycle i.e. you stimulate the
woman to produce the follicles and then you
use a drug that makes it burst so you are
even more precise in the timing of the
insemination.
In addition there is the advantage of skipping the
problematic cervical-vaginal passage for
spermatozoa.
The success rate in a good center is around 18-19%.
The success instead of in vitro fertilization is on
average 25%, but this considers all inseminations in
all age groups; it is much higher in the 18-25 age group (up to 65%).
The prognostic factors are related to the diagnosis, age and duration of sterility because couples who have been
trying for just one year have much more chances than couples who have been trying for 12 years. In addition,
the number of cycles IUI made is prognostic: the percentage of success is maximum at the first attempt,
decreases and then remains stable until the fourth
cycle, but then decreases more and more. That's
why you don't do more than six cycles.
What do you use to induce follicular growth?
1. Clomiphene citrate, an antiestrogen,
should be taken from the third to the
seventh day because it lowers estrogen
levels to create positive feedback on FSH
which increases to grow follicles to
produce estrogen. That way you "screw the
ovary" to work. This maximum for three
cycles is then no longer worthwhile and it
is better to use gonadotropins (urinary or synthetic).
2. Gonadotropins are produced at low doses by young women who only need a few to stimulate the
ovary, while many are produced by menopausal women because the ovary does not work and
therefore increase in an attempt to stimulate it. The first gonadotropins were produced by purification
from the urine of menopausal women (the professor states that they were initially produced by
collecting urine from menopausal nuns in the convents). Since 1992 there are also synthetic
gonadotropins which are more expensive (but the NHS passes it on). A low initial dose is given to
stimulate ovulation, but only for IUI and not for natural intercourse because the cost is not justified by
low success rates.
Patients should be monitored with both
ultrasound and blood samples and treatment
should be discontinued if there are more than 3
follicles growing otherwise there is a high risk of
twin pregnancies. In the 70-80s this precaution
was not taken and there were women who also
had 7-8 twins, but these pregnancies do not
usually end well some die in the first trimester.
[The professor tells about the Giannini family
who had had 7 twins because of the clomiphene
had become famous and did commercials]
Advantages of IUI: simplicity of execution, low
invasiveness and low cost
Disadvantages: multiple pregnancies due to super ovulation.
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Savoy Cabbage Andrea 19-11-

2019
Hajdukovic Dejan Gynaecology, Lesson
14
Prof.
Ambrosini
CERVIX CANCER
Cervical cancer is a particular type of cancer that should interest us because it is one of the few cancers that
can be prevented and potentially eradicated. In fact, this tumor in Western society has been tamed with a
simple test: the pap test. This is an easy, quick, painless, inexpensive, and inexpensive examination that allows
for extraordinary prevention. Today only foreign women living in countries where there is no prevention are
operated on cervical cancer, where the cancer can develop to advanced stages.
Cervical cancer of the cervix is still the 3rd most frequent cancer of the female reproductive tract with 370,000
cases per year in the world and the 2nd most frequent cause of death from cancer in women with 190,000
deaths per year in the world (this is because in many countries there
is no prevention and therefore still a lot of deaths). In Italy there are
fortunately only 3700 cases/year many linked to immigration.
Risk factors: HPV is the main risk factor, there are about 200
isotypes of which about fifty are sexually transmitted, the most
dangerous are 16, 18, 31, 33, 35. The transmission is sexual. The
risk increases with the number of sexual partners and
immunosuppression, smoking leads to a weaker immune system and
thus facilitates infection.
Signs and symptoms: often asymptomatic but may have mucous

vaginal discharge, spotting (modest blood loss between two menses),
post-coital vaginal bleeding. These symptoms are often
underestimated by patients because they often mean absolutely
nothing. The cervix fortunately has excellent accessibility and thanks
to the speculum I can see it easily (with the naked eye). I can also see
it with colposcopy, I can do a cytological screening by taking the
flaking cells, I can do a biopsy, I can palpate the lesion.
If I detect a precancerous lesion, I can easily remove it.
Histologically, 80% of these tumors are scaly and 15% are adenocarcinoma or adenosquamosis. In the early
stages surgery or radiotherapy is sufficient, while in the advanced stages radiotherapy is required (recently it
has been proposed to combine radiotherapy with cisplatin chemotherapy). Today, however, many fewer
cervical cancers are treated and operated on than in the past because prevention works.
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Staging:
 0: carcinoma in situ (intraepithelial)
 I: carcinoma limited to the cervix
 II: carcinoma affecting the cervix and
lower third of the vagina
 III: there is extension at pelvic level
 IV: extension to adjacent or distant
organs
The staging is mainly clinical and is done with bimanual

vaginal examination (involving both vagina and rectum),
colposcopy with biopsy on area that I consider at risk,
endocervical curettage, chest x-ray, cystoscopy and
proctosigmoidoscopy if suspected invasion.
One of the simplest but also most radical interventions

when we are at stage 0 is the conization that allows to
make a cone of tissue going to completely eliminate the
diseased part of the tissue. If the lesion is deeper,
obviously the only solution will be radical surgery with
removal of the organ.
Staging should always be done before starting any therapy and should be done immediately after diagnosis.
Very important is the lymph node state which is the most

important prognostic factor related to survival and
relapse. N+ obviously worsens survival, if I have
negative lymph nodes (N-) in fact survival is practically
90% while if lymph nodes are positive it drops to 50%.
[in the slide obviously N+ and N- are reversed]
If there are metastases or high stages, survival is very
low. At stage III-IV, which were most situations seen
before screening and before prevention, almost all
patients died. These patients presented only when they
had annoying symptoms such as pain or metrorrhagia or
symptoms related to the infiltration of other organs (all very late symptoms).
The prognosis also depends on the depth of stromal
invasion, the horizontal extension, the size of the tumor (I
can often feel a barrel neck if the tumor is large enough),
the lymphatic or blood diffusion, the histological type, the
degree of differentiation.
Therapy:
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 Stage Ia1: I can do the conization avoiding to mutilate the pz and therefore allowing the woman to
have a pregnancy in the future (both natural and assisted). The chance of death is <1% because the
chance that the tumor is not well staged with the conization cone is very low and the chance that it
spreads with metastasis is almost zero. If the pz already has children or is in menopause and does not
need the uterus I can also opt for a more
radical surgery such as extrafascial
hysterectomy PIVER I (i.e. a clean
hysterectomy without removing anything
else).
 Stage Ia2: the situation gets complicated, the
conization in this case must be evaluated with
the patient, it is done if the woman wants to
have children, but in this case close follow-ups
will be necessary. In all other cases, a PIVER
II hysterectomy is recommended because
already at this stage the risk of metastasis is 7-
8% and the risk of death is 2-3%.
 Stages Ib and IIa: PIVER III hysterectomy +
pelvic lymphadenectomy + radiotherapy,
survival >90%. Obviously it will be influenced
by the condition of the pz, age, etc..
Neoadjuvant chemotherapy does not change prognosis and survival. Adjuvant chemotherapy can
help.
Piver classification: there are 5 classes that classify the various types of
hysterectomy (enlarged or not)
 Class I: sufficient to remove neck or neck and uterus. I do an

extrafascial hysterectomy where I remove all the cervical tissue
and the body of the uterus.
 Class II: removal of the uterine body and paracervical tissue without altering the vascularization and
innervation of ureters and bladder, removal of even 1/3 of the upper part of the vagina. This doesn't
pose a problem for sexual intercourse
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 Class III: extensive parameter and paravaginal tissue removal

and removal of pelvic lymph nodes. I remove all the
paracervical tissues and also remove about half of the vagina.
 Class IV: uterine organ removal + periureteral tissue + perivaginal tissue + ¾ vagina. You can't spare
the bladder artery.
 Class V: distal recurrences involving also distal ureter or bladder.
Ureteroileoneocystostomy. Ѐ a stage more pertinent to general
surgery than gynaecology.
Radiotherapy: for stages IIb to IV, it should also include regional

parameters and lymph nodes. At the same time I can use cisplatin for one
week or cisplatin + 5-FU for 3-4 weeks. The advantages of chemotherapy
are only available if it is used as adjuvant therapy for surgery or
radiotherapy.
Follow up
About 35% of patients have persistent disease or will have relapses. The
risk of recurrence is higher in the first 2 years after treatment and this is
a "good thing" because in the first years the patient is very attentive to
her state of health while after 4 years you forget about the disease, you
think you are cured for good. Even from a psychological point of view a
disease that recurs after many years is devastating.
The follow-up includes visit + pap test every 3 months for the first 3
years, then every 6 months until the 4th-5th year, also 1 Rx chest per
year.
Cervical adenocarcinoma is not a contraindication to hormone replacement therapy.
Recidivism
The patient who has a relapse unfortunately has a low chance of survival.
Survival at 1 year is in fact 10-20%. If there are distant metastases the
situation is even worse. Rescue surgery with anterior, posterior or total
pelvectomy is attempted. In practice we do extremely mutilating
interventions, I have to remove rectum, colon, bladder; it changes a lot the
quality of life of the patient and sometimes even these interventions are
not enough to save her. That is why prevention is important. Very
advanced stages, however, are no longer seen today, even the non-EU
population that in the country of origin did not get checked in fact when it
comes to Italy begins to get checked and therefore never develops too advanced tumors.
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In Veneto
25 years
ago the
Women
project was
established, the region has started to send all women a

letter to invite them to take a free pap test. The pap test
was then advertised by newspapers, televisions, etc. and so today all the women who receive the letter for the
pap test go to do it. Today there is also the vaccine for non-valent HPV which is administered to females as
well as males if they wish, possibly within 15 years of age.
Cervical cancer during pregnancy

2-4% of invasive cervical carcinomas were diagnosed during pregnancy because the women did not make
check-ups and therefore the first visit to the gynaecologist was made during pregnancy and at that time the
cancer was found. Today this hardly happens anymore because it is impossible for a woman not to visit a
gynaecologist within 30-40 years. Today, prevention is one of the most important tasks of the gynaecologist.
Most women diagnosed with cancer during pregnancy are at stage I and have an 80% survival rate. But today
they are very rare thanks to the pap smear test. When they are found you have to assess what to do according to
the week of gestation. If you are at the beginning of pregnancy you can make a conization so as not to
compromise the pregnancy. If you are at an advanced week you can give birth and then, during the same
operation, hysterectomy + lymphadenectomy (then if necessary I will do radiotherapy or chemotherapy).
Questions:
1) Why is imaging not taken into account much in staging?
Because, at least at the initial assessment stage, I can see the tumor directly thanks to the position of the cervix
which is easily accessible. Then, after the diagnosis, we normally do chest X-ray, CT scan to better frame the
pz and see any extension of the tumor.
2) For a girl of 20-25 years old who has not been vaccinated for HPV does it make sense to get vaccinated?
Yes it makes sense to get vaccinated (3 injections in 6 months). Even if you have already had sexual
intercourse and have encountered an HPV virus you cannot know which type you have come into contact with.
If I also do a pap test or an HPV test I may be healthy but I may have caught the virus and passed the
infection, or I may test positive for a certain type but nothing prevents me from contracting a different type in
the future. So the vaccine is always useful, it can protect me from all types of HPV that are part of the vaccine
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or those with which I have not yet come into contact. In principle, according to the professor, it is advisable to
recommend the vaccine for HPV up to 30-35 years then not. From 40-50 years on, in fact, what is taken is
taken and sexual activity should be more contained and less at risk at these ages. The vaccine in adulthood,
however, is subject to payment (then depends on the individual regions until which age is free or at a reduced
price).
Pap test
Pap smear is the collection of cells that flake in the cervical mucus. This collection is done with a plastic or
wooden spatula. The mucus contains the cells and is then crawled onto a slide and stained with Pap. The slide
is then examined under the microscope for the first signs of pre-cancerous lesions. Ѐ easy to do and not painful
(then of course it depends a bit on the hand of the doctor who performs the examination).
Reduced cervical cancer mortality by 70%. Start with sexual intercourse and repeat every 1-2 years (also in
relation to the level of risk). The sensitivity is very high and reaches 75-90%. In 7-20% of cases it can give
false positives and in these cases it is therefore necessary to use second level tests such as HPV test or
colposcopy.
Through colposcopy, which allows us to enlarge the uterine port, we can also do a biopsy and then take a piece
of tissue.
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Colposcopic picture: usually the altered areas are areas where the epithelium is free of glycogen, so this
Schiller's test ensures that the dye is not detected in that area because atypical cells are present.
We can have an intraepithelial carcinoma (NPC) that does not cross the basal membrane, or we can have an
invasive carcinoma that crosses the basal membrane.
Intracervical neoplasia:
 is a clinically unproven injury,
 the diagnosis is only instrumental (through a colposcopy/biopsy),
 severity is variable from 1 to 3 (CIN 3 starts to be a problem because it is an in situ carcinoma, so it
has to be removed),
 is easily eradicated because you see it in front of you during surgery.
Squamous carcinoma, adenocarcinoma and mesenchymal tumours (e.g. rhabdomyosarcoma botrioid) are
malignant tumours that require major surgery.
Cervical cancer (80% of cases are squamous cell carcinoma) has decreased significantly over the last 30
years thanks to prevention, i.e. the early detection of precancerous lesions that is done with the Papanicolau
test (Pap-test). The Pap-test allows you to understand if there is an alteration, while with the biopsy you then
go to assess the depth of the invasion.
Stage Ib is a stage in which a major surgery is already needed, it is a tumor that only affects the portio but
which, although smaller than 4 cm, is still a tumor already large. It requires a hysterectomy and also the
removal of a piece of vagina. When we are in stage Ib the situation is already heavy, with a much lower
survival rate than stage Ia. At the visit you can feel a huge neck, defined as a "neck in a barrel".
Stage IIa at the visit does not create any kind of problem, but requires hysterectomy and vagina removal.
In stage II b at the visit you feel that a part of the vagina and the porthole are swollen and rigid, so you can
have a suspicion already at the visit.
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Finally, there are the metastatic stages: the metastases are primarily to the lung and liver.
OVARIAN CANCER
Ovarian cancer is a sneaky, malignant, sometimes fast tumor.
 It is the leading cause of death for gynecological tumors and
 the fifth leading cause of death among all cancers in women.
For this type of cancer, unfortunately, there is no instrument as easy and simple as the Pap-test, which allows
us to discover a pre-cancerous lesion.
A study has recently come to light for which there are patients who have specific mutated receptors, which
greatly increase the chances of having ovarian cancer and breast cancer --> are BRCA 1 and BRCA 2. For this
reason many people in the USA have decided to have this expensive blood test to see if they are carrying
mutations of these two genes (e.g. Angelina Jolie, being positive, decided to remove both her mammary glands
and her ovaries).
 In Europe it accounts for 5% of all female cancers,
 in Italy affects about 4000 people every year.
Basically, that means that when you catch him, you catch him late and the chances of death are pretty high.
"Classification's a bit difficult, but I'd like you to learn it by heart."
 Coelomatic epithelium tumors,
 Germ cell tumors,
 Tumors from the cells in the casket and the granulosa,
 Hilar and stroma cell tumors.
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Unfortunately, when you go to open a woman with an important tumor, you are faced with the real face of the
tumor coming out of the organ itself, which attacks all the surrounding organs and structures and which is
particularly aggressive and difficult to eradicate.
The neoplasms derived from the celomatic epithelium are the ones we see the most, especially serous tumors
and mucinous tumors.
Germ cell-derived neoplasms we see a little less of them, often they are tumors related to pediatric age.
Neoplasms derived from specialized gonadal stroma cells are rarer and, finally, neoplasms derived from non-
specialized gonadal mesenchyme are extremely rare.
This type of cancer metastasizes the gastrointestinal tract (stomach, colon, pancreas), lymph nodes, breast,
uterus and thyroid.
 Luckily for us, most of these serous tumors are benign serous cysts (every time you see a ball in the
ovary doing the ultrasound, it is a serous cyst that is absolutely benign); other times this type of serous
tumor needs more attention from the ultrasound specialist because this cyst can have borderline
characteristics, and other times it can have malignant characteristics instead.
 A 10% of these neoplasms are mucinous tumors, and again they can be benign, borderline or
malignant mucinous.
 Tumors that originate from germ cells are tumors that fortunately can be discovered through alpha-
fetoprotein and chorionic gonadotropin because they are tumors that produce these two substances;
they are typical of childhood and adolescence, so many times they are discovered in the emergency
room and not by the gynecologist. Teratoma is a benign tumor that usually affects adolescents, only
in rare cases has malignant changes; it is a particular tumor, in whose context we can also find
structures such as hair, teeth and bones.
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 Then we have stromal tumors, which are those originating from specialized and unspecialized
gonadal stroma, and which account for 4% of ovarian neoplasms; most are granulosa-stromal cell
tumors.
Epidemiology
Overall, ovarian cancer is a tumor with a low prevalence but high mortality: these are tumors that affect
women around the age of 50, mostly Caucasian.
Epidemiology depends on genetic predisposition, nutrition and reproductive history.
Risk factors
As far as the risk factors are concerned:
 Age: the likelihood of getting sick increases with age (for most cancers in general, the more alive you
are the more likely you are to get sick) in most cases ovarian cancer appears in women after
menopause, while it is infrequent before the age of 40.
 Familiarity: Women with familiarity or positive personal history for one of these tumours (uterus,
breast, colon rectum) need genetic counselling.
 Genetic factors: I told you that if BRCA 1 (90%) or BRCA 2 (10%) have mutated, the patient will be
3-5 times more likely to develop ovarian or breast cancer; in families expressing these BRCA 1 and
BRCA 2 there is a 50% and 26% risk of developing ovarian cancer by the age of 70, respectively.
 Endocrine and reproductive factors: the risk is higher in the case of early menarche and late
menopause the risk is directly related to the ovulatory period, i.e. the number of ovulatory cycles; is
instead inversely related to the number of pregnancies and breastfeeding (for this reason in the past,
when it was normal for a woman to have even 10 or more children and stay 10 or more years without
using the ovary, women had a lower probability of getting ovarian cancer; in today's society the
women who manage to "mimic" this are those who take estroprogestinics).
 Environmental factors: Medium-high socio-economic status leads more easily to this disease,
smoking, alcohol, a diet rich in lipids and poor in vitamin A (the latter factor is a bit ambiguous, as
usually a "fleshy" woman is reminiscent of endometrial cancer, while a skinny/casceptic woman is
reminiscent of ovarian cancer), asbestos and talc, ionizing radiations (the use of ionizing radiation for
diagnostic or therapeutic purposes does not seem to increase the risk ovarian radiation damage
depends on the cumulative dose, the extent of irradiation and the age of the patient).
Protective factors:
 Multiparity,
 Breastfeeding,
 Prolonged use of estroprogestinics,
 Bilateral adjectomy.
 One thing we haven't said: 80% of ovarian tumors are from the tuba, so hypothetically, if we removed
the tuba from all women without removing the ovary, we would almost eradicate the ovarian tumor.
Spreading:
 Direct dissemination (by contiguity): uterus, tubes; parietal and visceral peritoneum, peritoneal fluid;
omentum; intestine, appendix;
 For lymphatic and peritoneal fluid transport: paracolic showers; subdiaphragmatic and hepatic
surface;
 Lymphatic pathway: retroperitoneal, para-aortic and para-caval lymph nodes;
 Bloodway: liver, lungs, pleura, bones.
Clinic:
 In most cases at the beginning there is a blurred, paucisymptomatic clinical picture (he is a silent
killer);
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 pain appears when it's too late, only in acute complications;

 there may be an increase in the volume of the abdomen due to ascites or tumor mass, but this also
appears only in the more advanced stages;
 alterations to the bowel;
 emaciation (ovarian facies).
 in 75-80% of cases the disease has already advanced to diagnosis,

 in 10% of cases the diagnosis is made at stage I (occasional diagnosis),
 in 10% of cases the disease is limited to the pelvis at diagnosis.
Complications:
 Twist on the pedicle (pain can lead to the patient being examined earlier, leading to an earlier
diagnosis),
 Rupture of the cyst (also in this case there is pain, but it is a worse situation than the first because it
usually leads to great dissemination),
 Endocystic bleeding,
 Suppuration,
 Malignant degeneration of benign tumor.
Diagnosis
The diagnosis is usually random. The majority of diagnoses are made by transvaginal pelvic ultrasound,
followed by MRI or CT scan (all preceded, of course, by a gynaecological examination).
 Important: there are also tumour markers, especially CA125 and HE4.
Other diagnostic tools are laparoscopy and hormonal assays (in case of suspected functioning cancer).
Licci Giuseppe, Giuseppe, 01/10/2019

Laserra Piergiorgio Alberico Gynaecology, lez 15
Prof.
Ambrosini
TUMORS OF THE OVARY, BODY OF THE UTERUS, VAGINA

AND VULVA
OVARIAN EPITHELIAL
TUMORS
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In this lecture, we'll conclude the ovarian cancer first.

Environmental and genetic risk factors, signs and symptoms, diffusion have already been addressed.
[Editor's note: the professor only treats epithelial tumors and
teratoma in ovarian cancer, to have a general idea I enclose the
image of the classification. In general during the lesson he skipped
many slides, it might be useful to have a look at them in depth].
Diagnosis
The diagnosis is made by clinical examination, ultrasound, CT and
MRI scan, tumor markers, but then definitively made by surgery and
histological examination.
With the clinical examination of the abdomen and pelvis we try to
understand if there is a mass, if the uterine organ and the organs I can
palpate are fixed or mobile, if there is a peritoneal effusion. Then
these sensations will be confirmed with the ultrasound: a
gynaecologist normally does not use the ultrasound immediately
starts with the examination, gets an idea of the situation and the
ultrasound helps to understand exactly what the problem is. Many times this is enough, other times other tests
may be necessary. The ultrasound allows to evaluate ovarian lesions, and liver and peritoneal effusions;, in
addition, the ultrasound allows to understand the neovascularisation of some masses, which can be potentially
malignant. If anecogenic (potentially serous) and not vascularized it is very likely to be a benign disease.
Cancer markers are not helpful in early detection, but they are very interesting to follow up. In particular,
Ca125 is used to determine whether the disease is still present or not. In some tumors it may also be useful to
look at beta-HCG and alpha-fetoprotein.
CT scan and MRI allow staging of the neoplasm by understanding the relationship with neighbouring organs
and evaluating possible metastases.
The laparoscopy before was absolutely not recommended, today in expert hands it is a great resource, because
it allows to do the staging and to operate, in difficult cases it allows to pass to the laparotomy. The ovary in
fact is particularly difficult to operate in laparoscopy:, the possibility of disseminating is enormous and, the
tumor should be operated by very experienced hands because there are no large spaces in laparoscopia.
Oggi in veneto non esiste, ma proprioPrecisely for this reason it would be nice to have a regional pole
completely specialized in gynaecological oncological surgery. Today there is no such thing in Veneto, but Ma
asome particularly difficult tumours should be treated in a specialist centre. It would not be right for the heads
of small centres to do these particularly difficult operations without detracting from their abilities. Only a pole
that operates daily in difficult cases can give the best assistance, even in terms of pre- and post-intervention.
This is what's going to happen.
Here, for example, we have the reality of IOV as far as the breast is concerned, most of the oncological breasts
in the region are sent there.
Gynaecology is a fantastic branch that can do a thousand things, most gynaecologists know how to do
everything, but it is also right that pathologies of this type go into super-specialisation.
This is the classic ovarian cancer disseminating tissue aggressive

enough
Staging (FIGO)
The first stage is limited to the ovaries, the second extends to the
pelvis, in the third stage I have peritoneal metastases, while in the
fourth stage I have distant metastases (excluding peritoneals).
The teacher says that leggeremo reading the staging independently
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Remote dissemination can affect the brain, bones, pleura, liver and lung.
The most important prognostic factors are:
 The size of the disease
 The extension at the time of diagnosis
 The degree of differentiation. It is especially important in the early stages of the disease, because in
the advanced stages the tumor is almost always at a low degree of differentiation.
 Old age leads to worse prognosis
 the isotype, e.g. the light cell variant is particularly aggressive, but then each case is quite separate.
Treatment
The primary treatment is surgical, if not in very experienced hands directly in laparotomy with total
hysterectomy with bilateral annexectomy. The omentum, appendix, pelvic and lumboaortic lymph nodes
must also be removed.
It is necessary to study all the zones also with biopsy if necessary, someone says that it is necessary to study
the tissues up to the diaphragmatic dome, with also the exploration of the peritoneal free fluid, because these
patients always have ascites
In the case of giovani conyoung women with favourable prognostic factors, conservative therapy with
removal of only the affected gonad can be carried out, while the uterus and contralateral ovary are preserved.
This is a case to be reserved for young women who want to have children, otherwise the surgical treatment is
more complete.
 Poorly differentiated stage Ia or IB-Cc patients should also be treated with adjuvant cisplatin
therapy. In this tumor, adjuvant chemotherapy makes sense, unlike portio tumors.
 In stages II and IIII FIGO the therapy is radical surgical + chemotherapy
 In more advanced stages where surgical therapy is not possible, polychemotherapy (cisplatin+ taxol)
is the treatment of choice, possibly followed by surgical therapy.
Radiotherapy considered to be salvage in inoperable and non-responsive to chemo, but in general radiotherapy
does not belong to ovarian cancer.
The professor invites us to read the rest of the slides or we can't treat the other tumors.
Given the short lectures, you won't ask us about a random tumor, but you should read them because , it's also
interesting, maybe we like the subject and we can take it as a topic of pleasure.
Teratoma
It is a type of tumor with a terrifying ultrasound appearance, but it is actually a tumor of young women
absolutely benign, it is just very visually impactful.
UTERINE BODY TUMORS
Before moving on to the tumors of the vagina and vulva which interest us relatively little because they are rarer
(the professor says he has never seen one of the vagina), let's move on to a classic gynaecologist's tumor, that
of the uterine body (the uterine neck has already been addressed last time)
We can tell the difference between uterine tumors:
 Cervical cancer (cervix)
o Benigni: cervical polyp
o Malignants: cervical carcinoma
 Tumors of the body of the uterus
o Benign: myomas, polyps, endometrial hyperplasia
o Malignants: endometrial carcinoma
In cervical cancer the woman does not have a facies, in the sense that the patient has nothing particular at
firsto glance,sguardowhile in advanced ovarian cancer it is almost always a woman who has an ascites and a
cachectic face.
Women with uterine body cancer (type I endometrial cancer) are almost always a bit fat and often diabetic.
Endometrial octopus
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It's a benign tumor of the body of the uterus. A huge number of women produce polyps, some produce polyps
that are eliminated with menstruation, other polyps nobody will see them, others (only a small part)
degenerannowill be worthy., ma sono una minima parte
They can be single or multiple, the symptoms are blood loss, the diagnosis is usually made by ultrasound and
confirmed by hysteroscopy.
The octopus can be removed hysteroscopically and the surgery is quite easy, I certainly
do not remove a uterus for an octopus. Vaginal ultrasound looks pretty good. It's a ball
in the endometrium. You can tell if it is sessile or has a fairly important basic implant,
you can measure it.
This is instead a polypid endometrium
Miomi (fibromyomas, fibromyomas, leiomiomiomi)

They are benign tumors derived from muscle or connective tissue cells that form the myometrium.
Fibroids are hard nodules and are particularly annoying submucosal in fertile times because they can affect
fertility.
They are classified according to the percentage of the tumor protruding into the uterine cavity
 G0: they flow almost completely into the uterine cavity
 G1: half and half
 G2: much of it is in the muscular
This is a pedunculate fibroma, it's so voluminous but surgically it's very easy to remove.
This is una donnaa uterus with a lot of fibroids: it has a lot of G0 and
subsierositis at the bottom of the uterus.
This is a colliquated myoma: instead of an
entirely rigid mass (almost all the fibroids
we find) it is limp when touched, open it
is either emptied or has sticky liquid.
Malignant tumors
Endometrioid adenocarcinoma includes 75% of malignant
tumors in the body of the uterus, then there are other adenocarcinomas: those that produce mucin, those with
clear cells. Then we have carcinomas and sarcomas, which are less frequent but more dangerous, more
aggressive and faster growing.
Endometrial adenocarcinoma
Carcinoma of the endometrium is the most frequent gynaecological neoplasia in Western countries, it seems to
be related to obesity, diabetes, many carbohydrates, so it is more frequent in countries with a particularly
disorderly diet
There has been an increase in incidence in recent years, welfare has led to this type of problems. Most affected
women are between the ages of 45 and 65.
Etiopathogenesis
It seems to be particularly related to exposure of estrogen not related to progesterone (type I). Other risk
factors are obesity, diabetes, late menopause, familiarity and Tamoxifen (therapy in breast cancer).
There's a hormonal influence on carcinogenesis. When there is a hormonal dysfunction with exaggerated
estrogen production, this affects the endometrial receptor which leads to endometrial hyperplasia, which
becomes adenomatous and can become endometrial cancer. Also in this case, having the gynaecologist check
up with periodic visits can find precancerous forms saving vitàlives.
Taking cells is not as easy as in cervical cancer. Here at the ultrasound I can see if the endometrium is not
normal, but then I need hysteroscopy to see the endometrium and do the biopsy.
Endometrial hyperplasia
Endometrial hyperplasia is an increase in endometrial size. The experienced sonographer sees it very easily. It
is obvious that an endometrium of this type is extremely suggestive in a woman in menopause. And fortunately
it is a tumor that affects a perimenopausal woman, a woman who should have a silent endometrium, so it is
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extremely easy to make a diagnosis.Infatti In fact if it was in a woman with a cycle you could confuse
endometrial hyperplasia with an endometrium in advanced secretive phase, which does not look the same but
looks a lot like it. Then it's women who have blood loss, who don't want to say anything in a woman who
menstruates (often they bind to endocrine problem), but it's obvious that abnormal uterine bleeding (AUB) in
menopausal women immediately raise alarm for a precancerous lesion.
The etiology is related to the overproduction of estrogen unbalanced by progesterone.
Postmenopausal ovaries produce androgens that in fat patients in adipocytes are transformed into estrogen,
which can bind the endometrium receptor and modify cells. Endometrium can have simple hyperplasia, which
can become a glandular-cystic hyperplasia adenomatousatypical E.I.N 1-2-3 (E.I.N. as C.I.N.
classification for the cervix, but here I speak of endometrium not cervix) invasive carcinoma
Type I and Type II
AndMa ealso fix an endometrial carcinoma of senility (>70 years old,
endometrial carcinoma type II). It is not related to obesity and diabetes, but
to oncogenic factors. It is much worse: because it is much more silent, it is
much more difficult to see and it affects women who generally do not get
checked up: most women in fact, they visit up to 65 years old, then they
forget about the gynaecologist and their genitals.
ButMbetween cervical and endometrial cancer do not occur in this age
group,d’età , those of the ovary and especially of the uterus can happen
occasionally.
The tThypo I carcinoma will catch it and allows us to get good results saving
women, the tThypo II will not catch it and we will make a bad impression.
.
The professor then reads this table on the
different characteristics between type I and
type II.
Today there is a lot of talk about genetic
mutations, but it is also true that if I control
all genetic mutations I can have many
diseases, but only in power: it is still too early
for these markers to mean exactly having the
problems, there is more than one probability.
This can be useful, but it is important that the
person then knows how to emotionally
manage the information of the mutated gene..
Dissemination
The tumor spreads by continuity (verso
latowards the cervix, tubes, myometrium),
lymphatic (to the paraortic and pelvic lymph
nodes) and blood (to the lung, liver and bones).
Histological type
The mMaggior part is endometrioid, usually in a circumscribed,opseudopolopoid, infiltrating form..
There is also a widespread and vegetating form.
Macroscopically it looks like a cauliflower, difficult to forget it once youcsee
it, but it is also true that suggestive shapes like those of the image are difficult
to see today: now there is a different culture, so when you feel sick you
immediately show yourself.
Symptoms
What saves in type I is the metrorrhagia that occurs when the tumor is still in
its early stages: - the bleeding is a bit alarming to anyone- che si presenta
quando il tumore è ancora in fase iniziale. I can also get some leukoxantorrhea
and pelvic allergies.
Diagnosis
186X
The diagnosis is made with transvaginal ultrasound, hysteroscopy possibly with biopsy and scraping.
This picture is wrong. It's not a menopausa ,menopausal endometrium,

there are three laminas, like the periovulatory phase. In menopause the
endometrium must be linear, there must be a thin line, maximum 5 mm
long.
It's not normal for a woman in menopause to have an
endometrium like this.
Thisqsecond image is the classic periovulatory
endometrium display, it looks like a mouth,. The
woman must have così,valtrimentisuch an
endometrium, otherwise there is a situation of non-
synchrony between endometrium and ovulatory period.
In this third image we see the
difference between the atrophic endometrium in
a perimenopausal woman and the thickened
endometrium that alarms and requires
hysteroscopy.
Endometrial bBiopsia has limited reliability, it

is often painful, the information is sectorial and I
do not have an overview of the situationThis
means that if you enter with the Novak, a tool
that picks up blindly, you might not even pick up
the right material.
With hysteroscopy there has been a great
evolution in diagnostics, because it allows us to
take exactly what we want.
STADIAZIONE FIGOStaging FIGO

We have stages 0 through IV.
Stage 0 has atypical adenomatous hyperplasia or
carcinoma in situ, it is difficult to distinguish, but has a
very good prognosis.
Stage I does not exceed myometrium. Read the picture
for details.
InIn stage II the endocervical muscular invasion is
present, in stage III the serosa is invaded, with possible
vaginal, pelvic and paraortic lymph nodes
metastases.degli organi pelvici.
Stage IV has an invasion of rectum, sigma, tenuous and
distant organs such as bone and lung.
5-year survival in situ is 100%. For this reason in the last

few years there is a tendency to remove it
hysteroscopically, but in reality it is a dangerous pinch,
while if I remove the uterus I am very calm. In stage I
survival is still very high (70-98%), until it decreases in
the other stages.
187X
The beautiful thing is that theMovarian cancer is not immediately diagnosed, the endometrial cancer è
trovatois found very early and women do not die.o.
The difference is made by the prevention, in the endometrial cancer there is actually no prevention, but it
bleeds immediately, for the neck of the Uterus there is the PAP test and it is impossible to die, while iin the
case of ovariani cancer dell’ ovaiothe woman could also have a check-up every 23 years bute could be
particularly unlucky with development of tumor between visits.
Therapy
Every gynecological tumor is treated a little differently.
Carcinoma of the endometrium requires surgery at every
stage of the disease, with a total abdominal hysterectomy
+ bilateral adneectomy and lymphadenectomy. Someone
exports even a small piece, but it must only be done in
expert hands and is not by world literature. . Then I can do
adjuvant radiotherapy when the tumor becomes more
important, while chemo has no application, although there
are some schools of thought that do..
Recurrences occur more frequently in the vaginal dome,

pelvis, paraortic and distant lymph nodes (lung and bone
metastases)..
Uterine sarcomas
Uterine sarcomas are aDmalignant generation of stromal and muscle cells in the myometrium. The problem
with these tumors is that on ultrasound they have Sall’eco dei miomi, fibroids, but they are fast growing balls
and the prognosis is very bad. The sonographer must be careful because the possibility that a diagnosis of
fibroma is a sarcoma, even if minimal, there is. While in the fibroma you see the patient after one year, in this
case you would need a closer examination at 3 months to see if the mass has remained stable.
Sarcomas account for 1-3 % of malignant tumours in the body of the uterus, prof. has seen few,, dipende anche
come sono. c
Cbasically around the age of 504.
We distinguish
 Leiomyosarcomi (< 54 years)
 Endometrial stromal sarcoma
o Low grade (<50 years)
o High grade ( >50 years)
 Mullerian mixed sarcoma affects at 63-68 years oldil sarcoma stromale endometriale può essere di
bass
la clinica è caratterizzata da una diffusione rapidissima
The symptomatology is often non-specific and vaginal blood loss is
actually very rare. There may be a feeling of weight and pain due to the
contraction stimulated by the tumor that tends to stretch the muscle
fibers.
Other symptoms are fever, pelvic pain, anemic state, rapid increase in
uterine volume. The consistency is also indicative: you feel a big and soft
uterus, very ugly, if it was hard I would think invece adinstead of a
fibroma.Comportamento clinico aggressivo 54£
It has a very rapid diffusion by blood, lymphatic, by contiguity.
188X
53% have aggressive clinical behaviour, with 14% local pelvic recurrence and 33% distant metastasis.
Leiomyosarcoma
Non abbiamo neanche il tempo di
Characteristic of young women under 40 years age, they can have mixoid modifications, with margin
infiltration and vascular invasion and have a
particularly aggressive biological behavior., sono t
Endometrial stroma moods Tare very molto rareoand of little mi interessainterest to us.
Sarcoma therapy
In generali.
Low grading hysterectomy with bilateral

attachments
In high-grade sarcomas I can addAd alto grado faccio
stesso + LA chemotherapy and radiotherapy.
(reagisce anche male, ma necessaria)
Chemo that is not done for endometrial tumors is done
for sarcoma, which is a much more aggressive tumor,
which reacts to chemo, even if it is bad, but you can't
do anything else because it metastasizes very easily.
TheSmedian survival is al primoat stage one 52

months, in stage two 16 months. We're talking about a
completely different uterine tumor, with very different
than endometrial cancer.
When we make a diagnosis we already know what survival is, in the endometrial tumor the patient is saved,
who does not know that it is a cancer in which surgery can do so much. That'sit's a cancer that will make the
gynaecologist look good and save the patient. . In sarcoma, on the sappiamo cheother hand, one goes into
surgery knowing already lathat surgery will do little good.
The risk of recurrence is enormous. It's a tumor it's always best not to trip over.
VULVA TUMOURS
The vulva is a way to classify all the small areas that are below theal Mount of Venus. We have, for example,
the foreskin of the clitoris, the clitoris, small and large lips, the urethra. They areTalla a series of structures that
for the ordinary citizen are vagina, but for the doctor they are vulvaper noi sono vulv. And even these areas can
get sick
The professorIo remembers a pimpleo on her big lip,7 casi in tutto il mondo, that was not actually a pimple
and the woman diedlin a year and a half. The strange lesions on the vulvar level Dobbiamomust be given the
dignity they deserve.
Tutte queste zone si possono ammalare. These tumors can also loro spread by continuitòcontinuity,
contiguitacontiguity and blood and lingticalymphatic.
189X
This is
a vulva removing fat and skin, here I see how it is
done, there are a series of muscles and organs.
Poi Arteries che carry blood are branches of internal
pudenda. verso lap pudenda interna.
Some vulvar diseases are not necessarily precursors

cancer, but in any case, care must be taken..
The absolute disease to valurtareevaluate that could
become malattia degenerative of the vulva is lichen
(sclerosus, planus and chronic simplex).
There may also be hyperplasia and other dermatoses, which should not be a cause for alarm, but should make
the woman visit at least once a year.
These alterations are psoriasis, boiling pemphigus, seborrheic dermatitis.
. All these vulvar lesions could somehow degenerate. These pre neoplastic lesions sono lesioni che are also
called with an acronym, which is not C.I.N (cervical), not E.I.N (endometrial), but V.I.N (I-II-III).
Con The biopsy sample allows to see if this tissue has been affected only partially, completely or even if it is a
lesion that has passed the junction is therefore a fully invasive carcinoma. It is definitely dangerous, not like
the ovary but still very dangerous, the lìunicaonly good thing is that it affects olderpersne people, the
emotional impact is definitely less..
It is a tumor that can be undiagnosed easily perchebecause the senile population is less attentive to new things,
less controlled and less worried.
In fact, a tumor of the vulva should be easily identifiable due to its external position, but the lack of interest of
older people means that it is not diagnosed in time.
Among the vulvar intraepithelial neoplasms we can recognize:
190X
 Squamous intraepithelial neoplasia

o VIN I = mild dysplasia low number of atypia confined in the lower III of the epithelium
o VIN II = mean dysplasia atypia extend 2/3 of the epithelium with low frequency of
individually keratinized cells and mitosis above the basal layer
o VIN III = severe dysplasia or carcinoma in situ almost the entire epithelial layer is involved
 Non-squamous intraepithelial neoplasia
o Paget's disease
o Melanoma in situ
Some VIN III, such as cervical diseases, may be related to HPV infection; these types of lesions have a rather
positive prognosis due to the high tendency to spontaneous regression. Nevertheless, any type of injury,
whether VIN III or CIN III, should be treated.
Non HPV-related forms of VIN III have a much worse prognosis and tend not to regress but rather to evolve
into invasive carcinoma.
Among the histological characteristics of VIN it is possible to highlight bizarre giant cell mitoses [Professor
claims that this data interests us relatively little].
Risk factors associated with the possible appearance of a VIN are:
 Immunodepression and associated increased frequency and severity of infections
 Hyperplastic dystrophies
 Viral infections
o HPV (Type-16 and 18, the most oncogenic)
o HSV 2 [the professor claims that HSV does not appear to be an important risk factor since
he has never seen a neoplastic evolution caused by this virus].
 Sexually Transmissible Diseases (the reference is in any case to HPV, since a Candida or Chlamydia
infection does not cause transformative lesions)
 Previous CIN or VAIN
 Pregnancy [NdA, the professor says he does not know how pregnancy can affect the increased
incidence of VIN].
Clinical picture
In 25% of the cases there are no detectable skin abnormalities, while in the remaining part of the cases it is
possible to highlight highly different lesions (papular, warty, hyperpigmented, hyperkeratosic, erythroplastic).
Professor's anecdote: At the beginning of his career he happened to find a vulvar lesion that he thought was of
little medical importance. Luckily the pz returned to his attention for other reasons the following month and,
noticing an increase in the size of the alteration, he turned to a gynaecologist expert in vulva.
In young patients the lesions are usually multicentric, while in patients over 50 years of age they are usually
unicentric.
Important from the symptomatological point of view is the itching: this is the reason for presenting the pz to
the doctor. Associated with itching are scratching lesions, which can easily be seen during inspection. Despite
this, about 30% of patients are asymptomatic.
In order to make the diagnosis, both the medical history and the objective examination are helpful and the
biopsy allows a precise diagnosis to be made. In order to better inspect the vaginal lesions, it is possible to use
the microscope usually used for colposcopy.
Evolution of VIN III
The possibility of regression is only attributable to HPV-related injuries. Otherwise:
 In the absence of treatment
o 16.6 % of the cases are transformed into invasive carcinoma.
 After treatment
o 3-4% can evolve into invasive Ca
o In 15-50% of cases there may be recurrences; therefore it is not an easily treatable tumour.
Treatment
Usually the treatment is articulated as an excision with a lozenge-shaped incision of the skin, superimposable
on the procedure used for the removal of the nevi.
In the slide below are represented all therapy approaches
191X
The treatment is chosen according to the degree of the lesion and the patient's characteristics.
 VIN I and II attendant/medical/surgical conservative VIN I and II
 VIN III Conservative Surgical VIN III (scalpel, laser, radiofrequency)
The characteristics of the patient to be taken into consideration for the implementation of a treatment are the
following:
Exclusionary Demolition
Age > 45 years Age < 45 years
Pz immunodepressed Chondilomatous-like lesions
Syndylodystrophic lesions Multifocal lesions
Unifocal lesions Mucosa or glabrous skin
Extensive injuries Periurethral/perianal lesions
Cute furry
Carcinoma of the vulva

Epidemiology
There is a prevalence of 1.5 cases/100 000 women over the age of 60. It represents 3-5% of female malignant
tumors and almost all of them are flat epithelial carcinomas (melanomas, adenocarcinomas and sarcomas are
less represented).
Histological classification
Such neoplasms can be distinguished into:
 Skin and mucous membrane epithelial neoplasms
o Invasive scaly carcinoma
o Basal cell carcinoma
o Adenocarcinoma
 Bartolin's gland carcinoma (accessory gland)
 Carcinoma and ectopic breast tissue sarcoma
 Soft tissue sarcoma
192X
Association with HPV

Related HPV Not HPV related
General Tumours associated with HPV Tumours associated with
infection on histological squamous cell hyperplasia and
examination often have more or lichen sclerosus have invasive
less differentiated "intraepithelial- patterns with obvious
like" invasive patterns. keratinization and a worse
prognosis than HPV positive
tumours.
Genetic mutation p53
Frequency 30% 70%
Age Young Advanced
Precursors VIN Lichen sclerosus (it is important to
try to understand, in a pz with this
lesion, if there is a possibility of
tumor evolution)
HPV 16 75-100% 20%
Injury Multifocal Unifocal
Type of tumor Basaloid Squamous keratinizing
Smoking Yes No
Preinvasive lesion Yes No
Signs and symptoms

Usually the lesion presents as a small whitish thickened epithelial area that can progress to a fixed, hard or
ulcerated exophytic lesion. To the attention of a gynaecologist not particularly experienced in vulvar diseases,
these lesions could be assimilated to dermatitis or eczema. In the case of ulcerative lesions, the diagnosis can
also be made by doctors less experienced in this field.
Initially, the most frequent symptom is definitely itching, whereas in the case of ulcerative lesions, this
symptom can evolve into pain.
Spreading paths
193X
Staging
This is done through:
 Clinical examination:
o Injury monitoring and measurement
o Control of inguinal lymph nodes
o Assessment of local extension (vagina, urethra and anus)
 Cysto-rectroscopy
 Imaging Diagnostics
Classification
194X
Paget's disease
[NdA, the professor only hints at this pathology, reading the first two slides. Transcript of the slides below]
Paget's disease of the vulva is similar to Paget's disease of the breast and therefore presents as a red, irregular
area, well demarcated to map. Usually the lesion is located at the level of the large lips and is characterized as
a palpable submucosal thickening.
Paget's disease of the vulva is often confined to the skin and its appendages; it can persist for years, even
decades, without developing invasion.
Paget's cells also spread outside the boundaries of the obvious lesion.
Prognosis is bad if associated with carcinoma.
Vulvar Carcinoma Therapy
This image shows what the perineal situation looks like following removal of vulvar carcinoma. The vulva is
completely removed keeping the
vagina, with an aesthetic outcome
certainly poor. Despite this, this
type of cancer usually occurs in
older women who are no longer
very interested in the aesthetic
appearance of their genitals and
therefore the surgery does not
involve excessive mutilation. The
big lips are changed a lot while the
small lips no longer exist.
Follow up
195X
The follow up is done through:

 Clinical examination
 Cytology
 Vulvoscopy
 Restaging examinations; cystoscopy; rectoscopy; chest X-ray; urography; bone hepatic scintigraphy
VAGINAL CARCINOMA
General
It is very rare to detect the presence of primitive forms of the vagina while it is easier to detect the presence of
secondary forms spread by contiguity or by blood. Secondary tumours can therefore come from the cervix,
vulva, bladder and rectum as well as from an endometrial, breast or lung K.
Primary tumors include both carcinomas and sarcomas.
VAIN
Risk factors are:
 Pregnant gynaecological neoplasms
 Prolonged use of pessaries
o The pessary is an instrument that has fallen into disuse and that few older women still use
today. It is a concave rubber disc which is extensible but rigid at the same time to be inserted
inside the vagina and which, when stuck near the uterine port, prevents the prolapse of the
uterus to the outside of the vagina. Pessars in the long run lead to small lacerations with
consequent infections, inflammation and tissue reshaping.
 HPV infections
 Pregnant pelvic irradiation
The cytoarchitectonic alterations of the vagina are indicated by the acronym VAIN and, as for NICs and
VINs, here too we find stage I, II and III.
Again, injuries can be associated with HPV. The incidence of this type of lesion is therefore increasing, given
the increase in the incidence of MST in general. This is certainly due to new customs and traditions as well as
new types of infections that come through migration. Therefore, new generations will more easily develop
vaginal cancer: in addition to the risk factors mentioned above, there is certainly the impossibility to easily
notice the presence of a new lesion inside the vaginal canal.
The most common location is the rear archway.
The peak of maximum incidence is at 50-55 years of age because the woman probably contracted the infection
from a dangerous HPV at 25 years of age and, given the slow evolution, the neoplasm occurs 30 years later.
Diagnosis
The inspection of the vagina is not very easy to carry out and the situation does not improve using a speculum;
it is also difficult to distinguish the normal and characteristic wrinkles of the vagina from any injury.
However, once the lesion has been identified, it is first necessary to characterize the lesion using an in situ
microscope and then perform a targeted biopsy to allow us to understand the nature of the ongoing
pathological process, adding a typing of HPV to this examination.
Therapy
In the case of VAIN I or II it is necessary to remove the lesion directly, usually using a laser. A wider excision
should be performed in case of VAIN III by removing a lozenge of vaginal tissue. It may seem a relatively
simple operation, but the anatomical characteristics (physiologically closed channel) and spraying (very high
vascularization) make the operation slightly more complicated.
Vaginal carcinoma
This type of neoplasia is found more often in the posterior wall of the vagina and presents as a nodular
exophytic formation with ulcerations or as a stenuous endophytic form.
Microscopically, in most cases it is a spinocellular epithelioma.
There may be spread by contiguity at the urethra of the bladder and vulva and rectum, through the lymphatic
pathway to the lymph nodes obturator while, by blood (late) goes to the lung, liver and bones.
Symptoms
196X
Usually the patient doesn't have any major disturbances, but in the case of manifest symptoms, vaginal
bleeding as well as lecuoxanthorrhea can be detected. In the case of stage IV cancer, there may be additional
symptoms that are very suggestive, such as urinary and rectal disorders and pelvic pain.
Diagnosis
Vaginal carcinoma can be diagnosed by means of specular examination (preferably a transparent to a steel
speculum), colposcopy and vaginoscopy. Once the lesion has been identified, a biopsy and typing of HPV is
recommended.
Staging
It is carried out through clinical examination establishing the size and infiltration of the lesion, colposcopy,
CT, chest X-ray, cystoscopy and rectoscopy.
Therapy
Survival at 5 years
197X
Prophylaxis and prevention

 Treatment of HPV infection (mainly based on the implementation of immune system functionality)
 Follow up for pcs with previous CIN III, which have already undergone cervical removal but may
present an outbreak of local vaginal recurrence.
L neoplasia intraepiteliale può essere squamosa o non squamosa.

VIN I scarso numero di atipie confinaante nel III indferiore dell’epitelio
La vin II può essere associate all’HPV e hnno un’ottima tendenza alla regressione spontanea, ma non sempre,
comviene sempre fare la conizzazione. Esiste anche una Vin III non HPV correlata, non regredisce ed è un
tumore sucuramente più aggressivo.
Istologicamente ci interessa poco. Ci sono delle mitosi bizzare e cellule giganti
VIN: fattori di rischio. Immunodepresso, distrofie iperplastiche, infezioni virali (HPV 16-\8-31, ma anche
HSV2), malattie sessualmente trasmesse, gravidanza.
Obiettività:
nel 25% ho assenza anormalità
75% lesioni di aspetto variabile, cadiamo nel mondo della sfortuna di incontrare un ginecologo non esperto.
Lui qundo incontro questo tumore non diede nessun tipo di allarme, fortunatamente dopo un mese la signora
ritornò, era aumentata di volume, altrimenti.
Lèimportante è sentire la struttura nel tempo
Sintomatologia è prurito, se noi controlliamo e troviamo zone con lesioni legate al grattamnento, queste sono
degne di attenzione.
ANAMNESI
Qualcosa te la dice così come i sintomi, lìispezione ti dice molto peché le lesioni sono tante e possono essere
banalmente benigne
colposcopia
198X

Gineco ENGLISH

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Licci, Laserra Lez.

I - Gynaecology and Obstetrics Prof Ambrosini, 01/10/19

GAMETOGENESIS, FERTILIZATION, OVARIAN

Images of placenta, umbilical cord and

The oocyte has many layers, for example we have the

The egg is extruded from the ovary at the moment of

Why might the egg not come this far?

The spermatozoon is a Formula 1 machine. The

At a certain point there is the removal of the sperm

The nesting is nothing more than the

Distance between the two parietal bones

Invasion of the deciduous

Syndizotrophoblast formation of vascular gaps (Fig. 4)

Cytotrophoblast-deciduous connection (anchor villi)

Connection with maternal placental circulation vessels

Formation of the chorion internal surface trophoblast + extra-embryonic mesoderm

Secondary villi training

Tertiary villi training

Equipped with a vascular component

Formation of fetal-placental circulation

The fetal-placental circulation is

Hormonal changes during pregnancy

Inhibin and Activin

In figure the event of childbirth

Assessment of the presence and frequency of uterine contractions

Assessment of cervical dilatation

Fetal heart rate monitoring equipment

OVARIAN AND MENSTRUAL CYCLE

Menstrual cycle: monthly cyclic changes to the endometrium

FSH has small variations in concentration and a long half-life.

The professor says the estriol is of little

Casarotto Arianna 03-10-2019

OVARIAN CYCLE AND MATERNAL CHANGES IN PREGNANCY

DEVELOPMENT OF PRIMARY FOLLICLES

The menarche is the first day of menstruation, appears in most

In the initial recruitment, hundreds of follicles are recruited, and

After two cycles, there is the formation of the cavern and

At the beginning of the cycle some follicles

The maximum estrogen production will be

The endometrium represents that part of tissue

MATERNAL MODIFICATIONS DURING PREGNANCY

FEMALE GENITAL APPARATUS

CARBOHYDRATES AND PANCREAS

SKIN AND MUSCULOSKELETAL SYSTEM

Ruggero Lo Scalzo 08/10/2019

Pregnancy monitoring, obstetric and gynaecological ultrasound,

- Signs of presumption general maternal phenomena: the increase in the volume of

Risk factors for pregnancy:

1st midwife visit

Early obstetric ultrasound

Questions from the gynaecological visit

Examining also the presence of oedemas and/or varicose veins.

The mother only has to fatten up to a certain amount:

OBSTETRIC AND GYNAECOLOGICAL ULTRASOUND

Obstetric ultrasound and gynaecology is now the basis of gynaecology.

The ultrasound can be of two types:

What's the ultrasound for?

- To study the Fetal Annexes

Also important is the possible diagnosis of an ectopic pregnancy, a situation that

Ectopic pregnancy can be:

-Angular, near the tubular corners

- A possible corpus luteum (index that the patient ovulated)

- Bi wall diameter (BPD)

It is always important to make a :