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Flashcards in Session 4 Deck (63):

Q. Annotate the menstrual cycle

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•  Explain the processes involved in and control of ovulation LO

•  Explain the pattern of secretion of gonadotrophins and LO

•  Explain the hypothalamic and pituitary mechanisms underlying gonadal steroids over the normal menstrual cycle cyclical gonadotrophin secretion LO and the interactions between the ovaries and hypothalamus/pituitary LO

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•  Explain the changes occurring in the ovary during the ovarian cycle LO 

Give a brief explanation of the hisological changes 

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Decribe histology 

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Describe the histology 

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Describe the histology 

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Explain the hypothalamic and pituitary mechanisms underlying gonadal steroids over the normal menstrual cycle cyclical gonadotrophin secretion LO and the interactions between the ovaries and hypothalamus/pituitary LO


Draw the HPG axis in the female & male 

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Q. Describe the HPO Axis LO 


A. • GnRH produced by the hypothalamus 
• Acts on anterior pituitary to release gonadotrophins
– LH 
• Gonadotrophins act on ovary
– Promoting follicular development
– Production of ovarian hormones
• Steroid hormones 
• inhibin
• Controlled by effects of gonadal hormones
– Negative and positive feedback control


Q. 1. How is GnRH released? 
2. Why is this important? 
3. Clinical significance?


A. 1. Pulsatile GnRH release 
2. Intermittent GnRH receptor is an absolute requirement for fertility 
If GnRH receptors are exposed to continuous presence of GnRH they become desensitised 
FSH & LH production stops -> Gonadal steroid production stops.
3. Endometriosis -> Treatment with GnRH agonist to relieve symptoms
Sometimes want to switch axis of continuous supply of GnRH which desensitises the receptor 
No production of LH and FSH
No positive feedback on the ovaries
No production of oestrogen and progesterone 
Endometriosis is when plaques of endometrium grows – irritates peritoneum 
As it is endromentrium will grown when there is oestrogen and progesterone 
Oestrogen inhibited which inhibits oestrogen induced proliferation of the endometrium


Describe the phases of the menstrual cycle LO

Q. What is the menstrual cycle? (3)


A. • Preparation
– Of the gamete = Ovarian cycle 
– Of the endometrium = Uterine cycle

• Ovulation 
– Release of the gamete 

• Waiting
– Pause, maintaining the endometrium until a signal is received to indicate that fertilisation has happened


Q. The ovarian & uterine cycle is split into what phases?


A. Ovarian: • Follicular • Luteal
Uterine: • Proliferative • Secretory


Q. • Menstruation occurs on a monthly cycle throughout reproductive life unless interrupted by a pregnancy 
• Normal duration ? days 
• Variations in cycle duration due to variation in the length of the ?
• ? phase strictly controlled ? days


A. 21 – 35
follicular phase
14 +/- 2


Q. Factors affecting the menstrual cycle


A. • Physiological factors
– Pregnancy
– Lactation 
• Emotional stress 
• Low body weight


Q. What phases is the ovarian cycle split in? 


A. Menses, proliferative and secretory phase


Q. Explain the levels of hormones at the start of the Ovarian cycle 0-4 days (6)


A. Start of cycle
• No ovarian hormone production -> • Low steroid and inhibin levels 
• Early development of follicles begins 
• Little inhibition at the hypothalamus / anterior pituitary 
• Free from inhibition 
• FSH levels rising
(First day of menstraution endometrium has lost its trophic support)


Q. What are the effects of FSH 


A. • FSH binds to granulosa cells 
• Follicular development continues 
• Theca interna appears 
• Follicle now capable of oestrogen secretion 
• Inhibin secretion begins
(Granulosa cells and theca cells needed to make oestrogen)


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Label this image?

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Q. Adding subtle control – mid-follicular phase
We need to nominate a dominant follicle & prevent recruitment of any further follicles, how?


A. • Follicular oestrogen now at a conc when it can exert POSITIVE feedback at the hypothalamus & anterior pituitary 
• Gonadotophin levels can rise 
• Effect seen on LH only 
• Follicular inhibin rising
– Selective inhibition on FSH production by anterior pituitary


Q. What changes happen to prepare for ovulation ( I.e. changes in conc)


A. • Circulating oestradiol & inhibin rise rapidly 
• Oestradiol production no longer dependent on FSH (theca & granulosa cells?)
• Surge in LH production (positive feedback from oestrogen need surge in oestrogen to create an LH surge)
• Progesterone production begins
– Granulosa cells become responsive to LH 
• Modulation of GnRH pulse generator


Q. What is causing the change in the response of GnRH by LH?


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A. High [oestradiol] enhances sensitivity of anterior pituitary gondadotrophs to GnRH


Q. What happens in ovulation?


A. • Meiosis I completes & Meiosis II starts 
• Mature oocyte extruded through the capsule of the ovary


Q. What are the Effects of LH (5)


A. • After ovulation, the follicle is luteinised -> corpus luteum
• Secretes oestrogen & progesterone in large quantities 
• Inhibin continues to be produced (waiting phase prevents further gamete phase?)
• But LH is now also suppressed because of negative feedback due to the presence of progesterone (oestrogen + progesterone = negative feedback on LH or FSH or is it both??) 
• Further gamete development suspended
Waiting phase established


Q. Luteal phase
1. The Corpus luteum produces? 
2. Why does it regress? 
3. How long does it take to regress?


A. 1. progesterone & oestrogens from androgens • Produces inhibin • Promotes production of progesterone
2.  Regresses spontaneously in the absence of a further rise in LH
3. Stays alive for 14 days then will regress if no LH signal


Q. Uterine cycle
• The lining of the uterus, endometrium, is responsive to hormones produced by the ovary 
• The endometrium is a specialised epithelium 
• Responds to oestrogen by ?
• Responds to oestrogen and progesterone by ?


A. proliferating, secreting


Q. What two things can happen at the end of the cycle?


A. End of the cycle…..
• In the absence of a further rise in LH, corpus luteum regresses 
• Dramatic fall in gonadal hormones 
• Relieving negative feedback 
• Resets to start again

or not
• If fertilisation has occurred 
Syncytiotrophoblast produces human chorionic gonadotrophin (hCG) 
– i.e. made by the embryo to signal its presence 
• Exerts a luteinising effect



Q. If fertilisation does take place what continues the production of steroid hormones


A. • Corpus luteum, supported by placental hCG, produces steroid hormones to support the pregnancy 
• Eventually, the placenta is capable of production of sufficient quantities of steroid hormones to control the HPO axis throughout pregnancy


Q. What produces inhibin?


A. Granulosa cells 


Explain the actions of oestrogen & progesterone in the non-pregnant woman LO

Q. Which phase does oestrogen exert its affects? What effect does oestrogen have in the non- pregnant women? 


A. Follicular phase
• Fallopian tube function 
• Thickening of endometrium 
• Growth & motility of myometrium 
• Thin alkaline cervical mucus (promote spermatozoa into the tract) 
• Vaginal changes 
• Changes in skin, hair, metabolism


Q. Which phase does progesterone exert its affects? What effect does oestrogen have in the non- pregnant women?


A. Luteal phase 
• Further thickening of endometrium into secretory form 
• Thickening of myometrium, but reduction of motility 
• Thick, acid cervical mucus (Creates a physical barrier to entry to the female reproductive tract reduced risk of infection in the reproductive tract should pregnancy have occurred)
• Changes in mammary tissue 
• Increased body temperature 
• Metabolic changes 
• Electrolyte changes


Describe the changes in the endometrium LO

Q. Describe the (layers of the) uterine wall and state which layer is removed during mensuration


A. • M = myometrium
– Muscular wall 
• E = endometrium – epithelial lining
– Functional layer (F) is hormone responsive and is shed if no pregnancy occurs
– Basal layer (B) provides the source from which a new functional layer is developed

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Describe the histology of the endometrium in the uterus 

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Q. How does the uterus change over the menstrual cycle? What physiological processes occur? 


A. Early proliferative: glands sparse, straight 
Late proliferative: functional layer has doubled, glands now coiled 
Early secretory: endometrium max thickness, very pronounced coiled glands 
Late secretory: glands adopt characteristic “saw-tooth” appearance

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Describe common menstrual disorders and explain the pathophysiology of these conditions LO

Q. State common menstrual disorders (7)


A. • Amenorrhoea- primary and secondary 
• Oligomenorrhoea 
• Menorrhagia/ Heavy Menstrual Bleeding (HMB) 
• Dysmenorrhoea 
• Intermenstrual bleeding (IMB) 
• Dysfunctional uterine bleeding (DUB) 
• Premenstrual syndrome (PMS)


• Amenorrhoea- primary and secondary 
• Oligomenorrhoea 
• Menorrhagia/ Heavy Menstrual Bleeding (HMB) 
• Dysmenorrhoea 
• Intermenstrual bleeding (IMB) 
• Dysfunctional uterine bleeding (DUB) 
• Premenstrual syndrome (PMS)

Define the disorders above


 • Amenorrhea: absence of menstruation

• Primary amenorrhoea: failure to establish menstruation by 16 years.

• Secondary amenorrhoea: cessation of previously normal menstruation 

• Oligomenorrhoea: infrequent menstruation, >35 days ie 4-9x/year 

• Menorrhagia/Heavy menstrual bleeding (HMB): a complaint of for >/= 6 months excessive menstrual blood loss over consecutive cycles or >80 mls per menstruation. (Not just about volume)

• Dysmenorrhoea: pain during menses, associated with ovulatory cycles 

• Intermenstrual bleeding (IMB)

• Dysfunctional uterine bleeding (DUB): heavy and irregular menstrual bleeding that occurs secondary to anovulation. 

• Premenstrual syndrome (PMS): A cyclical disorder, occurring in latter half of the menstrual cycle. Symptoms could be physical or psychological and resolve with onset of menstruation.

• Premenstrual dysphoric disorder is the severe end of the spectrum with extreme mood symptoms e.g. homicidal feelings 


Q. Common causes of the disorders of menstruation (4+) LO


A. • Hormonal- HPO AXIS 

• Chromosomal anomalies e.g. Mayer-Rokitansky-Kustner-Hayer (MRHK) syndrome; XO- Turner’s syndrome; androgen insensitivity syndrome; Swyer syndrome, Congenital adrenal hyperplasia (CAH) 

• Structural/Anatomical- uterine or vaginal e.g fibroids, polyps. (If HPO axis normal most likely a structural cause) increase SA then heavy bleeding= polyps any part of female genital tract obstructed…

• Other:
• Bleeding diathesis 
• Drugs (Warfarin)
• Thyroid disease 
• Chronic illness


Q. What is turners syndrome?


A. Caused by Sex Linked aneuploidies: 45, X. ONLY IN WOMEN. Symptoms: short stature, webbed neck, low-set ears, renal problems, infertility, no mental retardation.
Streak gonads problem in the ovary 
High GnRH
No estrogen/ progesterone 


Q. What is Mayer-Rokitansky-Kustner-Hayer (MRHK) syndrome; 


A. Müllerian agenesis is a congenital malformation characterized by a failure of the Müllerian duct to develop, resulting in a missing uterus and variable degrees of vaginal hypoplasia of its upper portion. Müllerian agenesis (including absence of the uterus, cervix and/or vagina) is the cause in 15% of cases of primary amenorrhoea. Because most of the vagina does not develop from the Müllerian duct, instead developing from the urogenital sinus along with the bladder and urethra, it is present even when the Müllerian duct is completely absent. – secondary sexual characteristics are still present


Q. What is androgen insensitivity syndrome

A. A child born with AIS is genetically male, but the external appearance of their genitals may be female or somewhere between male and female.
There are two main types of AIS, which are determined by how much the body is able to use testosterone. These are:
complete androgen insensitivity syndrome (CAIS) – where testosterone has no effect on sexual development, so the genitals are entirely female
partial androgen insensitivity syndrome (PAIS) – where testosterone still has some effect on sexual development, so the genitals are often between male and female
PAIS is usually noticed at birth because the genitals appear different.
CAIS can be more difficult to spot, as the genitals usually look normal for a girl. It's often not diagnosed until puberty, when periods don't start and pubic and underarm hair doesn't develop.


Q. What are streak gonads?


A. Extremely hypoplastic (underdeveloped) and dysfunctioning gonads mainly composed of fibrous tissue because of the progressive loss of germ cells on the developing gonads of an embryo. i.e., a form of aplasia in which the ovary is replaced by functionless tissue.


What is Swyer syndrome

A. a type of hypogonadism in a person whose karyotype is 46,XY. The person is externally female with streak gonads, and if left untreated, will not experience puberty.

The first known step of sexual differentiation of a normal XY fetus is the development of testes. The early stages of testicular formation in the second month of gestation requires the action of several genes, of which one of the earliest and most important is SRY, the sex-determining region of the Y chromosome. Mutations of SRY account for many cases of Swyer syndrome.

When such a gene is defective, the indifferent gonads fail to differentiate into testes in an XY (genetically male) fetus. Without testes, no testosterone or antimüllerian hormone (AMH) is produced. Without testosterone, the wolffian ducts fail to develop, so no internal male organs are formed. Also, the lack of testosterone means that no dihydrotestosterone is formed and consequently the external genitalia fail to virilize, resulting in normal female genitalia. Without AMH, the Müllerian ducts develop into normal internal female organs (uterus, fallopian tubes, cervix, vagina).

A baby who is apparently a girl is born and is normal in most anatomic respects except that the child has nonfunctional streak gonads instead of ovaries or testes. As girls' ovaries normally produce no important body changes before puberty, a defect of the reproductive system typically remains unsuspected until puberty fails to occur in people with Swyer syndrome. They appear to be normal girls and are generally considered so.


Q. What is congenital adrenal hyperplasia (CAH)


A. several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of mineralocorticoids, glucocorticoids or sex steroids from cholesterol by the adrenal glands (steroidogenesis). Most of these conditions involve excessive or deficient production of sex steroids and can alter development of primary or secondary sex characteristics in some affected infants, children, or adults.


Q. What is anovulation 


A. Anovulation is when the ovaries do not release an oocyte during a menstrual cycle. Therefore, ovulation does not take place. However, a woman who does not ovulate at each menstrual cycle is not necessarily going through menopause.


Q. Structural causes of menstrual disorders


A. • Agenesis/hypoplasia at any level of the genital tract 
• Leiomyoma- uterine fibroids (benign cancer of smooth muscle)
• Imperforate hymen, vaginal septae 
• Asherman’s syndrome 
• Cervical stenosis


Q. What is Müllerian agenesis?

A. - congenital malformation 
- failure of the Müllerian duct to develop = missing uterus and variable degrees of vaginal hypoplasia of its upper portion
- 15% of cases of primary amenorrhoea 


Q. What is an imperforate hymen? 


A. An imperforate hymen is a congenital disorder where a hymen without an opening completely obstructs the vagina. It is caused by a failure of the hymen to perforate during fetal development. It is most often diagnosed in adolescent girls when menstrual blood accumulates in the vagina and sometimes also in the uterus. It is treated by surgical incision of the hymen.


Q. How to diagnose?


A. cyclical pain, swelling abdomen 
transabdominal, transperineal or transrectal ultrasound


Q. What is this image showing? What imaging technique was used?


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A. Imperforate hymen & MRI


Q. What is this image showing?


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A. bulging blue membrane of the imperforate hymen 


Q. What are uterine fibroids?


A. are benign smooth muscle tumors of the uterus. Most women have no symptoms while others may have painful or heavy periods. If large enough, they may push on the bladder causing a frequent need to urinate. They may also cause pain during sex or lower back pain. A woman can have one uterine fibroid or many. Occasionally, fibroids may make it difficult to become pregnant, although this is uncommon.


Q. What are adhesions?


A. fibrous bands that form between tissues and organs, often as a result of injury during surgery. They may be thought of as internal scar tissue that connects tissues not normally connected.


Q. What is Ashermans syndrome?


- adhesions and/or fibrosis of the endometrium particularly but can also affect the myometrium

- associated with dilation and curettage (dilation (widening/opening) of the cervix and surgical removal of part of the lining of the uterus and/or contents of the uterus by scraping and scooping (curettage))  of the intrauterine cavity.


Q. What are the causes of amenorrhoea (primary or secondary) 

A. . • Amenorrhea: absence of menstruation

• Primary amenorrhoea: failure to establish menstruation by 16 years.

• Secondary amenorrhoea: cessation of previously normal menstruation 

• Physiologic causes: prepubertal; pregnancy; menopause 
• Pathology at the various levels of endocrine control: 
• Hypothalamic 
• Pituitary 
• Ovarian 
• Uterine/endometrial 
• Gonadotrophin levels indicate the level of the pathology


Q. Common causes of menorrhagia 

A. Menorrhagia/Heavy menstrual bleeding (HMB): a complaint of for >/= 6 months excessive menstrual blood loss over consecutive cycles or >80 mls per menstruation. (Not just about volume)
• Uterine fibroids- Leiomyoma 
• Uterine polyps 
• Endometrial cancer 
• Bleeding diathesis 
• Copper IUCD (birth control - Intrauterine device (IUD) with copper)
• Drugs- eg warfarin ( dosage may not result in the correct INR range)


Q. How do polyps cause menorrhagia  

A. Bleeding from the blood vessels of the polyp contributes to an increase of blood loss during menstruation and blood "spotting" between menstrual periods, or after menopause.


Q. Uterine fibroids may also be called uterine myomas or leiomyomas. The main types of fibroids are:


A. intramural fibroids – the most common type of fibroid, which develop in the muscle wall of the womb
subserosal fibroids – fibroids that develop outside the wall of the womb into the pelvis and can become very large
submucosal fibroids – fibroids that develop in the muscle layer beneath the womb's inner lining and grow into the cavity of the womb

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Q. What can cause irregular bleeding?


A. • Could present as a change in usual pattern 
• A feature of hormonal contraception, especially the progesterone-only preparations 
• Other causes: 
• STI’s/PID- infection 
• Cervical ectopy or pathology- usually as postcoital bleed 
• Endometrial pathology- polyp or cancer 
• Ovarian cyst – the hormone secreting type


Q. What are the two types of dysmenorrhoea? Associated with? 


A. Dysmenorrhoea: pain during menses, associated with ovulatory cycles 

• Primary is idiopathic, due to response of the uterus to local prostaglandins, hence painful contractions. Can be secondary to HMB. 

• Secondary can be due to endometriosis or obstructed menses (e.g. imperforate hymen)
• Associated with ovulatory cycles ( what does she mean by this? 


Q. What is endometriosis?


A. The layer of tissue that normally covers the inside of the uterus grows outside of it e.g. ovaries, fallopian tubes, and tissue around the uterus and ovaries
- pelvic pain and infertility. Nearly half of those affected have chronic pelvic pain, while in 70% pain occurs during menstruation
- Pain during sex is also common
- Infertility occurs in up to half of women affected

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1. PMS:

2. Common symptoms

1. Premenstrual syndrome (PMS): A cyclical disorder, occurring in latter half of the menstrual cycle. Symptoms could be physical or psychological and resolve with onset of menstruation

2. acne, tender breasts, bloating, feeling tired, irritability, and mood changes. Symptoms do not occur during pregnancy or following menopause.

• Is subjective

• Cyclical

• Can be distressing and even debilitating

• Severe form- premenstrual dysphoric disorder


Q. What should we target in the patients history 


A. Comprehensive history- 
emphasis on age; 
menarche/onset of puberty; 
pain- cyclical or not; 
menstrual history- cycle,
change etc; 
sexual history; 
medical history; 
symptoms of effects -> Anaemic, pale, tachycardia etc


Q. What should the examination entail?


A. - General, abdominal, speculum (dilates vagina for examination of the vagina and cervix), bimanual
• Presence or absence of secondary sexual characteristics, appearance of known chromosomal abnormalities or abnormal facies 
• Swellings/lumps/masses, discharge, pattern of hair growth

Gait, facial hair, do you have breast?
Swelling in abdomen -> imperforate hymen  
Turners webbed neck, short stature, large feet 

Masculine voice


Q. Investigations:

A. • Blood, hormone profile- gonadotrophins (FSH, LH); karyotype; thyroid function test, full blood count 
• imaging- USS, MRI
• Hysteroscopy- diagnostic and therapeutic (Camera inside the uterus (polyps) -> Fibroid which is dangling)
• Laparoscopy- diagnostic and therapeutic (Looks inside the abdomen 
-> quite invasive panoramic view of the pelvis, Uterus tubes endometriosis)


Q. How would you manage patients?


A. Management
• The goal of treatment is to correct the underlying condition 
• Part of management is the attitude to the patient- listen, empathy, acknowledgement of their symptoms. Be Humane. 
• Back to the HPO axis! 
• Pharmacological- use of gonadotrophins, progesterone, COCP/HRT 
• Surgical- depends on the condition
Psychological, social, physical effects!