GEP (Life Cycle Week 2) Flashcards

1
Q

What is the pelvic girdle/bony pelvis and what bones does it consist of

A

2 hip bones (aka innominate or pelvis bones)
Sacrum
Coccyx

The pelvic girdle or the bony pelvis is a bony ring, formed by the left and right hip bones and the sacrum, and it surrounds the pelvic cavity, and connects the vertebral column to the lower limbs.

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2
Q

What is the function of the pelvic girdle

A
  • Supports upper body weight
  • Provides attachment for a number of muscles and ligaments
  • Contains and protects the viscera
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3
Q

What are the 4 articulations within the pelvis

A
  • Sacroiliac joints (x2) – between the ilium of the hip bones, and the sacrum.
  • Sacrococcygeal symphysis –between the sacrum and the coccyx.
  • Pubic symphysis –between the pubis bodies of the two hip bones.
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4
Q

What are the hip bones and what are they comprised of

A

Two irregularly shaped bones that form part of the pelvic girdle
Comprised of three parts:
* Ilium
* Pubis
* Ischium

The hip bone is comprised of the three parts; theilium, pubis and ischium.Prior to puberty,thetriradiate cartilage separates these parts – and fusion only begins at the age of 15-17.

Together, the ilium, pubis and ischium form a cup-shaped socket known as the acetabulum. The head of the femur articulates with the acetabulum to form the hip joint.

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5
Q

What are the 3 main articulations of the hip bones

A
  • Sacroiliac joint – articulation with the sacrum.
  • Pubic symphysis – articulation between the left and right hip bones.
  • Hip joint – articulation with the head of femur.
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6
Q

What are the 4 main ligaments of the pelvis

A

Four main ligaments:
* Sacrotuberous
* Sacrospinous
* Iliolumbar
* Sacroiliac

The prefix is the insertion of the ligament, while the suffix is the origin of the ligament i.e. the iliolumbar inserts into the ilium, and originates in the lumbar vertebrae

The sacrotuberous and sacrospinous ligaments transform the lesser and greater sciatic notches into foramina.
The sacrotuberous ligaments run from the sacrum to the ischial tuberosity, forming the lesser sciatic foramen
The sacrospinous runs from the ischial spine to the sacrum, creating the greater sciatic foramen.
NB. Remember this for when we talk about the pudendal nerve and nerve blocks.

The sacroiliac ligaments (anterior, posterior and interosseous) are the strongest in the body.

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7
Q

What is the greater and lesser Pelvis

A

The osteology of the pelvic girdle allows the pelvic region to be divided into two:
* Greater pelvis (false pelvis) – located superiorly, it provides support of the lower abdominal viscera (such as the ileum and sigmoid colon). It has little obstetric relevance.
* Lesser pelvis (true pelvis) – located inferiorly, it contains the rectum, bladder, vagina, cervix and prostate. It has greater obstetric relevance.

The junction between the greater and lesser pelvis is known as the pelvic inlet. The outer bony edges of the pelvic inlet are called the pelvic brim.

The walls of the true pelvis:
Anterior: is the shallowest wall and is formed by the posterior surfaces of the bodies of the pubic bones, the pubic rami, and the symphysis pubis

Posterior: is large and formed by sacrum, coccyx , piriformis muscles and their covering of parietal pelvic fascia

Lateral: is formed by part of the hip bone below the pelvic inlet, the obturator internus and its covering fascia & the obturator fascia, the sacrotuberous ligament and the sacrospinous ligament

Inferior (aka pelvic floor): is a basin-like structure which supports the pelvic viscera and is formed by the pelvic diaphragm. It stretches across the true pelvis and divides it into the main (true) pelvic cavity above, which contains the pelvic viscera, & the perineum below which carries the external genital organs

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8
Q

What is the pelvic inlet and outlet

A

Pelvic Inlet
The pelvic inlet marks the boundary between the greater pelvis and lesser pelvis. Its size is defined by its edge, the pelvic brim.
The borders of the pelvic inlet:
Posterior–sacral promontory (the superior portion of the sacrum) and sacral wings (ala).
Lateral –arcuate line on the inner surface of the ilium, and the pectineal line on the superior pubic ramus.
Anterior –pubic symphysis.

The pelvic inlet determines the size and shape of the birth canal, with the prominent ridges a key site for attachment of muscle and ligaments.

Pelvic Outlet
The pelvic outlet is located at the end of the lesser pelvis, and the beginning of the pelvic wall.
Its borders are:
Posterior: The tip of the coccyx
Lateral: The ischial tuberosities and the inferior margin of the sacrotuberous ligament
Anterior: The pubic arch (the inferior border of the ischiopubic rami).

The angle beneath the pubic arch is known as the sub-pubic angle and is of a greater size in women.

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9
Q

What are the adaptation of childbirth

A

The majority of women have a gynaecoid pelvis, as opposed to the male android pelvis. The slight differences in their structures creates a greater pelvic outlet, adapted to aid the process of childbirth.

When comparing the two, the gynaecoid pelvis has:
A wider and broader structure yet it is lighter in weight
An oval-shaped inlet compared with the heart-shaped android pelvis.
Less prominent ischial spines, allowing for a greater bispinous diameter
A greater angled sub-pubic arch, more than 80-90 degrees.
A sacrum which is shorter, more curved and with a less pronounced sacral promontory.

In addition to the bony adaptations, the sacrotuberous and sacrospinous ligaments can stretch under the influence of progesterone and increase the size of the outlet further.

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10
Q

What is the perineum

A

Most inferior part of the pelvic outlet, separated from the pelvic cavity by the pelvic floor.

It’s the region between the thighs, that contains urogenital structures and the anus.

Diamond shaped region when the legs are abducted
Which can be further divided into two triangles- urogenital and anal triangles

with the perineal body at the junction between (often referred to as the perineum, however in anatomical sense this is not quite accurate). This is clinically relevant in labour and child birth, episiotomy.

There are 2 main ways to consider the borders: anatomical and surface borders

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11
Q

What is the pudental nerve, where does it arise from and its role

A

Nerve roots–S2-S4

Sensory–innervates theexternal genitaliaof both sexes and the skin around theanus, anal canaland perineum
Motor–innervates various pelvic muscles, theexternal urethral sphincter and the external anal sphincter.

Course-
Descends and exits the pelvis through the greater sciatic foramen
Crosses the sacrospinous ligament
Re-enters through the lesser sciatic foramen and then through
Courses through the pudendal canal

Thepudendal nerveis formed from the sacral plexus – a network of nerve fibres located on the posterior pelvic wall. It arises from the ventral rami (anterior divisions) of the spinal nerves S2, S3 and S4.

S2, S3, S4 keeps your poo off the floor

Sensory function:
Sensation to the genetalia and the skin in the area

Motor function:
The perineal nerve innervates muscles of the perineum and pelvic floor:
Bulbospongiosus
Ischiocavernosus
Levator ani muscles
The levator ani muscles also recieve innervation directly from the anterior ramus of the S4 nerve root

It first passes through the greater sciatic foramen, crosses the sacrospinous ligament and then passes through the lesser sciatic foramen which is formed by the sacrospinous ligaments as anna mentioned.
It then travels through the pudendal canal, also known as Alcocks canal, along with the pudendal artery and vein.

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12
Q

What are the branches of the pudental nerve

A
  • Inferior rectal nerve– innervates the perianal skin and lower third of the anal canal.
  • Perineal nerve– innervates the skin of the perineum, labia minora and majora or posterior scrotum.
  • Dorsal nerve of the penis orclitoris– innervates the skin of the penis or clitoris.

Clinical relevance -Pudendal nerve block is sometimes used in in vaginal childbirth and before episiotomies.

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13
Q

What is the pelvic peritoneum

A

Thin serous membrane lining the pelvic cavity.

Broad ligament:
Double layer of peritoneum covering the uterus and extending from the lateral pelvic walls
Supports the uterus, ligaments, the ovaries and the ampulla of the uterine tubes

Forms 2 pouches in the pelvic cavity; vesicouterine pouch & rectouterine pouch

Covers the majority of the female reproductive organs and part of the bladder

Rectouterine pouch (Pouch of Douglas) and Vesicouterine pouch
They serve as potential sites for fluid accumulation, such as in pelvic inflammatory disease, endometriosis, or ectopic pregnancy.

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14
Q

What is the pelvic floor and what does it consist of

A

A group of muscles and ligaments that support the bladder, uterus and bowel.

Consists of:
-Levator ani: puborectalis, pubococcygeus and iliococcygeus
-Coccygeus

Mnemonic for pelvic floor muscles: Could I Please Peak

-The pelvic floor also helps maintain urinary continence and faecal continence. The pelvic floor is a funnel-shaped structure which attaches to the walls of the lesser pelvis, separating the pelvic cavity from the perineum.
-Dysfunction can present as urinary/fecal incontinence, prolapse, pelvic pain or sexual dysfunction and can be due to obstetric trauma, increasing age, obesity and chronic straining.

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15
Q

What is a hysterectomy

A

Hysterectomy = removal of the uterus

Types:
Subtotal: removal of uterus
Total: removal of uterus and cervix
Radical: removal of uterus, cervix and part of the vagina (parametrium = connective tissue)
NB. Bilateral Salpingo-Oophorectomy = the removal of both fallopian tubes (salpingo-) and ovaries (oophorectomy) surgically

Indications:
Heavy periods
Dysfunctional uterine bleeding
Pelvic pain
Uterine prolapse
Ovarian, cervical or uterus cancer

Approach of procedure:
Abdominal: via an incision in the abdomen
Vaginal: via incision through the superior part of the vagina
Laparoscopic: via small incisions in the abdomen and using laparoscopes and a uterine manipulator

Complications:
Haemorrhage
Infection and DVT / PE
Bladder, ureteric or bowel injury

Recovery time - may be 6-8 weeks (less if laparoscopic/vaginal)

Side effects:
Temporary bowel/bladder disturbances
Vaginal discharge for up to 6 weeks
Menopausal symptoms
Emotional side effects – because of this, HRT can be used post hysterectomy (esp if ovaries are removed)

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16
Q

What is the cervix composed of

A

The cervix is composed of:
* The endocervical canal – mucus-secreting simple columnar epithelium
-Internal os
-External os
* The ectocervix – stratified squamous non-keritanised epithelium

The cervix
The cervix maintains sterility of the upper female reproductive tract
The cervix is composed of the endocervical canal and the ectocervix

The endocervical canal is bound by the internal and external os
It has a red, velvety appearance
The external os marks the transition from the ectocervix to endocervical canal inferiorly
The shape of the external os can have a circular appearance = nulliparous (pre-partum) or slit-like appearance = multiparous (post-partum)
It is made up of mucus-secreting simple columnar epithelium

**The ectocervix **is the distal part of the cervix which projects into the vagina
It has a pink appearance
It is made up of stratified squamous non-keritanised epithelium
This epithelium is resistant to the low pH of the vagina

17
Q

What is the SCJ and transformation zone

A

The squamocolumnar junction (SCJ)
Pre-menarchal = original SCJ
After puberty = new SCJ

The transition zone – where columnar epithelium undergoes squamous metaplasia

The squamocolumnar junction (SCJ)

  • The SCJ is the junction between the columnar and squamous epithelium of the ecto and endocervix
  • Pre-merchal, this junction lies close to the external os – called the original SCJ
  • The SCJ is actually a dynamic point that migrates under the influence hormones in puberty, pregnancy and menopause (as well as other hormonal stimulation)
  • After puberty, the female internal organs develop under influence of oestrogen and the cervix and uterus enlarge and cervix becomes more everted (ectropion), exposing more columnar epithelium to the low vaginal pH – this moves the original SCJ down
  • The Original SCJ moves back to where it was premenarchally after menopause
  • The transformation zone is where the columnar epithelium of the endocervix is exposed to the acidic vagina and undergo squamous metaplasia to be more resistant to the low pH – i.e. columnar epithelium is replaced with metaplastic squamous epithelium – this creates the new SCJ

IMPORTANT as in cervical cancer, microtrauma to the transformation zone cells provide HPV access and here accumulate mutations to cause CIN, and because of the already existing metaplasia, it puts this area at risk of dysplasia

18
Q

What is cervical screening

A

Offered to women/people with a cervix aged between 25-64
Sample of cells taken from the transformation zone
Checked for HPV/cell changes
HPV 16 and 18 high risk types

Cervical screening
Cervical screening (or smear test) is a test to check the health of the cervix and help prevent cervical cancer
It’s offered to women and people with a cervix aged 25 to 64
During the screening appointment, a small sample of cells is taken from the cervix, at the junction between the endo and exocervix (i.e. the transformation zone)
The sample is checked for certain types of human papillomavirus (HPV) that can cause changes to the cells of the cervix – high risk types are HPV 16 and 18
If someone is found to be HPV negative, is means the risk of getting cervical cancer is low, and they will be invited back in 3-5 years time (depending on age)
If someone is found to be HPV positive, there are two different outcomes:
If someone is HPV positive, with no abnormal cell changes, they will be invited for screening in 1 year (and 1 year again if there are still abnormal cells)
If there are abnormal cells after the 2 years, then they will be sent for colposcopy
If someone is HPV positive, with abnormal cell changes, they will be sent for colposcopy
NB. Colposcopy is a test where there is a magnified view of the cervix and vaginal tissue, allowing directed biopsy for pathological examination

19
Q

What is CIN in relation to cervical testing

A

Biopsy results may show cervical intraepithelial neoplasia (CIN) – this is not cancer, but instead shows that there are cellular changes to the ectocervix

Normal

CIN 1 (low grade) – up to one third of the thickness of the lining covering the cervix has abnormal cells
CIN 2 (high grade) – up to two thirds of the thickness of the lining covering the cervix has abnormal cells
CIN 3 (high grade) – the full thickness of the lining covering the cervix has abnormal cells

CIN 1 doesn’t normally need treatment as the cell changes often return to normal over time, CIN 2 may be monitored or treated, while CIN 3 is usually treated.

NB. Cancers of this area will be squamous cell carcinoma (80-90% of cervical cancers). You can also get glandular cell carcinomas (10-20% of cervical cancers), but they happen in cells of the endocervix.

20
Q

What is the menstrual cycle

A

Menstruation occurs on amonthly cyclethroughout female reproductive life.Menarche(the first menstrual cycle) normally occurs between the ages of 11 and 15 andmenopausebetween the ages of 45 and 55. The normal duration of a single cycle is21-35 days.

The cycle is regulated by an endocrine axis known as the HPG axis,Thehypothalamus, anterior pituitary gland and gonads(ovaries) work together
The hypothalamus releases GnRH which stimulates LH and FSH
These act directly on the ovaries

In childhood the the hypothalamus is inhibited from releasing much GnRH, about a year before menarche this changes, increased pulsitile release of FSH and LH which eventually initiates the menstrual cycle.

FSHbinds to granulosa cells to stimulate follicle growth, permit theconversion of androgens tooestrogensand stimulateinhibin secretion​.

LHacts on theca cells to stimulate the production and secretion ofandrogens

21
Q

How does the HPG feedback loop work in the menstrual cycle

A

HPG feedback loops:

Moderateoestrogenlevels- negative feedback
Highoestrogenlevels (in theabsence ofprogesterone) - postive feedback
Oestrogenin thepresence ofprogesterone – negativefeedback
Inhibinselectively inhibits FSH at the anteriorpituitary

The important thing is that the hormone Gonadotrophic releasing hormone is made and secreted from the hypothalamus

It then stimulates the anterior pituitary gland to release gonadatrophins- LH and FSH

These then act directly on the gonads, and in this instance on the ovaries, in order to facilitate the ovarian cycle.

The HPG axis is regulated by feedback and whether this is positive or negative feedback switches throughout the cycle.

Moderateoestrogenlevels- negativefeedback, which is occuring at the beginning of the cycle, during the oestrogen driven phase.

Highoestrogenlevels (in theabsenceofprogesterone) -postivefeedback, and this increased LH is what is responsible for ovulation

Oestrogenin thepresence ofprogesterone – negative feedback which is occuring the the secind half of the cycle, during the progesterone driven phase.

We will now go into more detail about the phases specifically.

Progesterone dominates in the second half of the cycle and its presence causes a reduction in the amount of oestrogen

22
Q

What are the 2 stages of the menstrual cycle

A

We are talking about 2 co- occuring cycles that work together

23
Q

What occurs in day 1-14 of the menstrual cycle

A

Follicular phase in the ovary
Day 1 of the menstrual cycle –> FSH rises (reduced negative feedback)
Rise in FSH → stimulation of ovarian follicles
Ovarian follicles grow → the level of oestradiol increases → negative feedback on the anterior pituitary
This inhibits the pituitary gland → FSH decline
FSH fall allows the selection of a dominant ovarian follicle
This follicle survives FSH fall due to increased FSH sensitivity and receptors, as well as increased numbers of granulosa cells
The granulosa cells also acquire LH receptors (switched on by FSH) which drives selection. There is a surge in LH which leads to ovulation.

Proliferativephase of uterus
Drives the stiatum functionalis to thicken

Day1 of the menstrual cycle –> FSH levels start torise

FSH leads to:
*thickeningof the endometrium
*renewalof connective tissue
*renewalof glandular structures

Oestrogenleads to:
*Endometrialstroma to deepen and become more vascularised

Follicular ohase:

As the last cycle has ended the Negative feedback has been switched off, allowing the anterior pituitary gland to release FSH and LH.
This stimulates ovarian follicles to develop, Only one dominant follicle can continue to maturity and be ovulated.
The developing follicles secrete oestridiol
As oestrogen levels rise, negative feedback reduces FSH levels, and only one follicle can survive, with the other follicles formingpolar bodies.
Follicular oestrogen eventually becomes high enough to initiate positive feedback at the HPG axis, increasing levels of GnRH and gonadotropins. However, the effect is only reflected in LH levels (theLH surge) due to the increased follicular inhibin, selectively inhibiting FSH production at the anterior pituitary. Granulosa cells become luteinized and express receptors for LH.

Proliferative phase:

Thestratum compactum and stratum spongiosum(which make up thestratumfunctionalis) begins tothicken, driven by FSH

24
Q

Describe Ovulation

A

Occurs approximately day 14
LH surge causes the dominant follicle to rupture, allowing the oocyte to exit the ovary
The fimbriae of the fallopian tubes help to sweep up the oocyte
Travels to the ampulla where it remains viable for 24 hours
What remains of the follicle in the ovary is now known as the corpus luteum

25
Q

What happens in day 15-28 of the Menstrual cycle

A

Luteal phase
Phase driven by CL
CLsecretes oestrogens, progesterone and inhibin
TheCL is maintained by LH and then bHCG following fertilisation.
No fertilisation->CL spontaneously regresses after 14 days
Regression stops –ve feedback and the cycle can begin again

Secretory phase
Progesterone from the CL stimulates myometrial and endometrial thickening
Mucous plug formation at the cervix
Changes to the mammary tissues and other metabolic changes

Luteal phase
The CL is made up of leutenised theca and granulosa cells (have been exposed to high levels of LH in the previous phase).CLsecretesoestrogens, progesteroneand inhibin to maintain conditionsappropriate forfertilisationandimplantation.

Luteal phase is always 14 days

The theca cells and granulosa cells allow the CL to produce progesterone and oestrogen. This exerts negative feedback on the hypothalamus, and LH and FSH levels are low during this time.
Progesterone causes de-differentiation of the ciliated cells in the fallopian tubes.

If there is no implantation, there is no bHCG and the corpus luteum dies after 14 days (turns into the corpus albicans). The levels of LH are low and cannot sustain the CL by itself. Consequently, progesterone production declines and disinhibits the anterior pituitary in the later luteal phase - this leads to a steady rise in FSH in the early follicular phase and the cycle continues.

The luteal phase is constant in most women - with a duration of 14 days. The variability in the cycle length is most commonly due to the follicular phase.

Secretory phase
Progesterone produced by the CL causes differentiation of the uterine endometrium, around 2-3 days after ovulation.
Causes a thick mucous plug at the cervix, which closes off the uterus to prevent poly fertilisation.
Cell division is reduced and glycoprotein/lipid secretion occurs, as well as increased vascular permeability and blood supply to endometrial cells.
Spiral arteries become coiled and grow rapidly. This all makes the endometrium favourable for the implanting of a potential blastocyst.
Also causes an increase in basal body temperature.
Othermetabollicchanges such asabdominal cramps, changes in mood,fatigue bloating etc.

Once the CL has regressed the drop in oestrogen and progesterone causes spiral arteries collapse, restricting blood flow to the stratum functionalis(most superficial layer of the endometrium) causing it to become ischaemic and necrotic → endometrium begins to shed

Bringing us right back to day 1- menstruation and the beginning of a new cycle.

26
Q

Define abnormal Uterine bleeding

A

Definition
Abnormal uterine bleeding (AUB) is the term used to describe any symptomatic variation from normal menstruation in terms of regularity, frequency, volume, or duration
AUB also includes symptoms of heavy menstrual bleeding and inter-menstrual bleeding (IMB)

Definition:
Abnormal uterine bleeding (AUB) is the term used to describe any symptomatic variation from normal menstruation in terms of regularity, frequency, volume, or duration
AUB also includes symptoms of heavy menstrual bleeding and inter-menstrual bleeding (IMB)

Different types of uterine bleeding (see table on slide)

27
Q

What are the causes of abnormal bleeding

A

Causes of AUB:
PALM-COEIN is a useful acronym provided by the International Federation of Obstetrics and Gynecology (FIGO) to classify the underlying aetiologies of abnormal uterine bleeding
The first portion, PALM, describes structural issues
Polyp
Adenomyosis – endometrial tissue growing into muscular wall of uterus
Leiomyomata – aka fibroids (v common)
Malignancy or hyperplasia
The second portion, COEI, describes non-structural issues
Coagulopathy
Ovulatory disorder
Endometrial
Iatrogenic
The N stands for “not otherwise classified”
Not otherwise classified

Causes can also be classified by:
Abnormalities of reproductive tract (endometriosis, fibroids, adenomyosis, infections, malignancy, polyps cervical or endometrial, trauma, benign pelvic lesions, PCOS)
Pregnancy complications (ectopic or molar pregnancy (abnormal fertilised egg implants into uterus, with unusual growth of cells, can become cancerous), spontaneous abortion)
Iatrogenic (contraception, IUD, anticoagulation, HRT, some psychiatric drugs (SSRIs, tricyclic antidepressants and antipsychotics))
Systemic disease (liver cirrhosis, coagulation disorder, hypothyroidism)
DUB - DUB is abnormal bleeding in the absence of structural or organic pathology. It is a diagnosis of exclusion. It is most commonly related to anovulation where the follicle does not release the egg and hormonal imbalance. It most commonly presents as menorrhagia and menometrorrhagia. 60% of menorrhagia is DUB!!!

28
Q

Not a question

A Summary of Uterine bleeding

A
29
Q

What are the treatment of abnormal uterine bleeding

A

Medical:
Hormonal
Mirena IUS
COCP
Progestogens
Non-hormonal
Antifibrinolytics (e.g. tranexamic acid)
Mefenamic acid

Surgical:
Endometrial resection/ablation
Hysterectomy
Oophorectomy

Treatment depends on the underlying cause for AUB – for example if the patient has fibroids, then these may be removed in order to control the AUB

Generally for AUB, treatment is split up into medical (hormonal and non-hormonal) and surgical

Medical:
Hormonal
Mirena IUS – 90% reduction blood loss
Uses the progesterone hormone levonorgestrel (which is also in the emergency contraception pill)
30% amenorrhoeic
Local high dose progestogen - thin endometrium
COCP – 20-30% reduction in blood loss
Removes cyclical events – thin endometrium
Progestogens used to control cycle length in anovulatory DUB
Non-hormonal
Tranexamic acid - anti fibrinolytics 40-50% reduction in blood loss
Corrects excessive fibrin breakdown in endometrium (affects plasminogen action)
Mefenamic acid 30% reduction in blood loss
It is an NSAID – corrects PG imbalance to allow normal vasoconstriction and platelet aggregation
Good for pain also

Surgical:
Endometrial resection/ablation
Hysterectomy - vaginal/abdominal
Remove ovaries

30
Q

Define Menopause

A

Perimenopause
The stage right before menopause
Can last up to 10 years
Usually starts when women are in their 40s
On average, lasts 4 years
Transitions to menopause when amenorrhea exceeds 12 consecutive months

Menopause
Menopause - defined after 12 consecutive months of amenorrhea
The woman stops menstruating monthly and she can no longer get pregnant
Average age in the UK is 51
Low oestrogen and progesterone, high LH and FSH

Post-menopause
Defined as the years after menopause occurs

Premature Menopause
Classified as menopause before the age of 45

Premature Ovarian Insufficiency
The ovaries no longer work before the age of 40

31
Q

What is the Physiology of Menopause

A
  • Ovaries becomes desensitized to LH and FSH
  • Less Oestrogen and Progesterone are secreted
  • LH and FSH rise unopposed, via the HPG axis
  • No inhibin is released due to no developing follicles, meaning that levels of FSH rise the more.

Impact of these physiological changes:

Shortened cycle
Absent ovulation
Menorrhagia
Infertility

impact on menstrual cycle:
Shortened cycle (early M)- Increased FSH leads to earlier oestrogen and LH surge which decreases follicular phase

Delayed/absent ovulation (late M)
Oestrogen production occurs earlier in follicular phase due to increased FSH but impaired granulosa cell function means levels are not high enough to induce LH surge

Heavier periods
Longer oestrogen stimulation of endometrium causing increased thickness and shedding during menstruation

Infertility
Increased miscarriage rate due to increased chromosomal abnormalities

32
Q

What are the presentation of Menopause

A
  • Reduced progesterone leads to skinwrinkling.
  • Symptoms are mostly caused by the reduction in Oestrogen
  • See symptoms in image ->
  • Increased risk of osteoporosis due to reduced oestrogen
  • Increased risk of cardiovascular disease

This decrease in estrogen production can lead to symptoms such as hot flashes, night sweats, vaginal dryness, and changes in mood and cognition. Estrogen also plays a role in maintaining bone density, so its decline can contribute to osteoporosis and bone fractures.

Oestrogen is also cardiovascular protective so there is incraesed risk of CVD post menopausally

33
Q

What are the treatment for menopause

A

Lifestyle measures
Regular exercise
Weight loss (if overweight)
Clothing alterations
Stress reduction
Avoiding triggers
Good sleep hygiene

Hormone replacement therapy

Other
Non-hormonal treatments
Non-pharmaceutical treatments
Behavioural therapies

Management options:
Lifestyle measures
Regular exercise
Weight loss (if overweight)
Clothing alterations
Stress reduction
Avoiding triggers
Good sleep hygiene

Hormone replacement therapy (will discuss on next slide)

Other
Non hormonal treatments
Clonidine
SSRIs
SNRIs
Gabapentin
Non pharmaceutical treatments
Phytoestrogens (oestrogen like compounds from plants) e.g. isoflavones, soya
Herbal treatments e.g. Black cohosh, Red clover, St john’s wort
Behavioural therapies
CBT
Hypnotherapy

34
Q

What is HRT (Hormonal Replacement Therapy), the benifits, risks, contraindications and administration option

A

Benefits
Control of menopausal symptoms
Maintenance of bone mineral density/prevention of fractures
Reduction in CVD
Improvement of muscle mass/strength
Protection against colorectal cancer

Risks
Breast cancer
Endometrial cancer (reduced by adding progesterone)
VTE
2-3x background risk
Not increased with transdermal HRT as bypass first metabolism by the liver, therefore does not effect the clotting cascade
CVD/stroke
Not increased with transdermal HRT

Contraindications
Current, past, or suspected breast cancer
Known or suspected oestrogen-dependent cancer
Undiagnosed vaginal bleeding
Untreated endometrial hyperplasia
Previous idiopathic or current VTE (deep vein thrombosis or pulmonary embolism), unless the woman is already on anticoagulant treatment
Active or recent arterial thromboembolic disease (for example angina or MI)
Active liver disease with abnormal LFTs
Pregnancy
Thrombophilic disorder

Administration options
Tablets (avoid systemic for those with hx of breast ca/hormonal susceptibility of breast ca)
Transdermal patches
Gel
Spray
IUD
Vaginal creams/tablets/rings for vaginal dryness

35
Q

What is the algorithm for HRT and indications for use

A

HRT
* Initial presentation with mild vasomotor symptoms
1st line: Lifestyle changes
* Women with a uterus + amenorrhoea >12 months (moderate to severe hot flushes, with/without reduced libido)
1st line: Continuous combined HRT
* Women with a uterus + perimenopause (moderate to severe hot flushes, with/without reduced libido)
1st line: Sequential combined HRT
Conjugated oestrogens/bazedoxifene
SSRIs/SNRIs
Gabapentin
Clonidine
* Women without a uterus or with an IUS (moderate to severe hot flushes, with/without reduced libido)
1st line: Oestrogen alone HRT
SSRIs/SNRIs
Gabapentin
Clonidine
* Urogenital atrophy only
1st line: Vaginal oestrogen +/- vaginal moisturiser
Ospemifene +/- vaginal moisturiser
* Urinary stress incontinence only
1st line: Pelvic floor rehabilitation

REMEMBER: individuals with a uterus need combined HRT (oestrogen and progesterone) – otherwise unopposed oestrogen increases the risk of both endometrial hyperplasia and endometrial carcinoma