Reproduction Flashcards

1
Q

Explain the pathway of a sperm.

A

They are synthesised in the seminiferous tubules. They then drain into:
- Straight tubules.
- Rete testis.
- Efferent ductules.
- Epididymis.
- Vas deferens.
- Ejaculatory duct.
- Urethra.

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2
Q

What are the two types of epithelium in the efferent ductules, and what are each of their functions?

A

Columnar ciliated epithelium - aid the movement of sperm.
Non-ciliated cuboidal epithelium - absorption of most of the fluid secreted by the seminiferous tubules.

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3
Q

What is the muscular coat surrounding in the seminal vesicles, and what stimulates it to contract?

A

It surrounds the glandular elements.
It is stimulated to contract by the sympathetic nervous system, during ejaculation.

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4
Q

What can happen to the glandular elements of the prostate in older men, and why?

A

They can become calcified, due to the content of calcium that it contains.

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5
Q

How do the testes descend from the abdominal canal?

A

During utero, through the inguinal canal, into the scrotum.

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6
Q

Where are the sperm cells stored before ejaculation, and what is its structure?

A

It is stored in the epididymis.
It has a head, a body and a tail.

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7
Q

What does the spermatic cord travel through?

A

The inguinal canal.

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8
Q

At which parts of the urethra are the internal and external urethral sphincters located?

A

Internal - pre-prostatic urethra.
External - membranous urethra.

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9
Q

What does the membranous part of the urethra pass through?

A

The deep perineal pouch.

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10
Q

What are the bulbourethral glands surrounded by, and what structure are they found in?

A

The external urethral sphincter.
They are found in the deep perineal pouch.

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11
Q

What do the prostatic ducts drain into?

A

The urethral sinus.

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12
Q

What parts and where do the corpora cavernosa attach to?

A

The crus attach at the ischial rami.

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13
Q

What is the bulb of the corpus spongiosum attached to?

A

The perineal membrane.

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14
Q

What makes up the base of the penis?

A

The crura of the corpus cavernosa and the bulb of the corpus spongiosum.

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15
Q

What does the suspensory ligament attach between?

A

The base of the penis to the pubic symphysis.

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16
Q

What does the fundiform ligament attach to?

A

The linear alba, to form a ring round the base of the penis.

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17
Q

What is the function of the testicular tunica albuginea?

A

Surrounding the seminiferous tubules to give structure, holding them together.

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18
Q

What is the function of the epididymis?

A

To store the sperm and facilitate maturation of them, allowing them to become motile.

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19
Q

What are the locations of the two cells associated with the seminiferous tubules?

A

The sertoli are found in the seminiferous tubule walls.
The leydig cells are found between the seminiferous tubules.

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20
Q

How do the Sertoli cells support spermtogenesis?

A

Removing cytoplasm, facilitating maturation.

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21
Q

What do the right and left testicular veins drain into?

A

The right testicular vein drains into the IVC.
The left testicular vein drains into the renal vein.

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22
Q

Why can inflammation of the lymph nodes supplying the testes not be felt?

A

The are para-aortic lymph nodes, which are deep within the abdomen and cannot be palpated.

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23
Q

What does the lymph from the scrotal skin drain to?

A

The inguinal lymph nodes.

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24
Q

What is the bell-clapper deformity, and what is the issue with this?

A

Where the tunica vaginalis completely envelops the testes and epididymis, increasing the risk of testicular torsion.

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25
Q

How does testicular torsion present as an emergency?

A

The twisting of the spermatic cord leads to compression of the venous and then arterial supply, leading to ischemia and infarction. This can lead to a decrease in fertility.

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26
Q

What can prevent testicular torsion from occurring again?

A

Suturing between the testicles and scrotum.

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27
Q

What does the gubernaculum do, and how does this occur?

A

It guides the testes from the abdomen into the scrotum.
It does this by the connective tissue attaching from the base of the scrotum to the lower pole of the testes.

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28
Q

What are the 3 fascias of the spermatic cord, and what are they formed from?

A

Internal spermatic fascia - transversalis fascia.
Cremasteric fascia - aponeurosis of the internal oblique.
External spermatic fascia - aponeurosis of the external oblique.

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29
Q

What is the motor nerve supply for the cremaster and what does stimulation of this do?

A

The genital branch from the genitofemoral nerve.
It contracts to pull the testicles up into the abdomen.

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30
Q

Apart from venous drainage, what is the secondary function of the pampiniform plexus, and why does this occur?

A

It has a concurrent flow to keep the testicular arteries cool.
This is because the optimum temperature for spermatogenesis is 35 degrees Celsius.

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31
Q

What parts of the prostate does benign prostatic hyperplasia (BPH) and prostate cancers effect?

A

BPH - transitional zone.
Prostate cancer - peripheral zone.

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32
Q

What does parasympathetic innervation to the penis cause?

A

Vasodilation of the arterioles and compression of the veins, resulting in erection.

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33
Q

What is the sympathetic innervation of the penis?

A

Vasoconstriction of the penile arterioles, leading to the termination of the erection.
It stimulates the ejaculation.

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34
Q

Why is there increased risk of varicoele to the left testicular vein?

A

The right testicular vein drains into the IVC at an oblique angle, as opposed to the left draining into the renal vein vertically.
There is an increased risk of pathology to the kidney, meaning the renal vein may become distended with an increased pressure.

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35
Q

Why do hydrocoeles often get bigger when coughing or crying?

A

There is an increased pressure in the abdomen, leading to fluid moving down into the tunica vaginalis.
This only occurs in children as there is still communication to the peritoneum.

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36
Q

How can a hydrocoele be distinguished from a tumour?

A

The hydrocoele will transilluminate.

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37
Q

What is the tunica albuginea of the penis, and what is the function of it?

A

A white sheet of elastic tissue that surrounds corpus cavernosa and corpus spongiosum.
This is to give the penis the cylindrical shape when erect.

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38
Q

What is a fractured penis?

A

Rupture of the tunica albuginea of the penis, leading to bleeding and deformation of the penis.

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39
Q

Why is knowing the angles between the vagina and cervix, and between the cervix and uterus important?

A

For IUD implants - making not to penetrate into or through the cervical or uterine wall.

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40
Q

Complete the following:

A
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41
Q

What can the sharp pain during ovulation be due to?

A

The egg bursting through the ovary, disrupting the capsule.

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42
Q

What is the main complications with ovarian cysts?

A

They can twist, forming ovarian torsion. This can cut off the ovarian and/ or uterine arteries.

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43
Q

What are the uterine and vaginal arteries branches of?

A

Internal iliac artery.

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44
Q

What connective tissue structure is the ovary held within?

A

Tunica albuginea.

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45
Q

What are ovarian cysts usually derived from, and what is the normal function of this?

A

Follicles of the ovary - stimulated by FSH to produce the primary follicle.

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46
Q

Describe the 3 components of the round ligament.

A
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47
Q

What is the remnant of the gubernaculum in females?

A

The round ligament.

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48
Q

Where do primordial germ cells originate from, where do they go, and how?

A

They originate from the endodermal yolk sac.
They go to the genital ridge, travelling along the dorsal mesentry of the hindgut.

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49
Q

What is the embryological origin of the genital ridge?

A

Intermediate mesoderm.

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50
Q

What forms the indifferent gonad, and what determines what gonad is formed?

A

Indifferent gonad is formed from the primordial germ cells and the primitive sex cords.
The presence of the SRY gene determines whether it will become testes. If it is absent then the ovaries will form (default).

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51
Q

What is the primitive sex cord formed from?

A

The proliferation of the genital ridges, penetrating the intermediate mesoderm.

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52
Q

What is required for the medullary cords to form, what are they made of and what do they become?

A

The SRY protein is required for their formation.
They consist of germ cells and Sertoli cells.
They become the seminiferous tubules.

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53
Q

What cells are seen between the medullary cords, and what are their function?

A

Leydig cells that produce testosterone.

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54
Q

In females, other than the ovary, what else is formed from the indifferent gonad, and what is their function?

A

Cortical cords - these surround the germ cells, forming the primordial follicle.

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55
Q

How does the paramesonephric duct form its products?

A

The two ducts fuse together, forming the uterus.
They also fuse to the sinovaginal bulb, forming the upper part of the vagina.
The remnants of the ducts form the fallopian tubes.

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56
Q

In Turner syndrome, 45,XO, what is the clinical presentation?

A

They have internal and external female genitalia.
They often have a wide neck and low set ears.
Amenorrhea.
Streak ovaries - wavy connective tissue.

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57
Q

How is Turner syndrome treated?

A

As oestrogen is not released, they are treated with hormone replacement.

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58
Q

What is the clinical presentation of Kleinfelter syndrome, 47,XXY?

A

Delayed puberty.
Small testes - hypogonadism.
Lack of male secondary sex characteristics with breast development.
Male internal and external genitalia.

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59
Q

In complete androgen insensitivity syndrome, what is the outcome of the ducts with 46,XY, why?

A

Neither mesonephric or paramesonephric ducts develop.
Mesonephric duct - the insensitivity to testosterone means that it does not develop.
Paramesonephric duct - the testes still produce MIH.

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60
Q

What is the clinical presentation of a patient with complete androgen insensitivity syndrome, 46,XY?

A

Male internal genitalia with female external genitalia.
They often develop a blind-ended vagina and breasts.

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61
Q

What is the function of Sertoli cells?

A

Provide nutrients and growth factors for the cytodifferentiation of indifferent gametes into sperm.
Help to form the blood-testis barrier, in the seminiferous tubules.

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62
Q

What do type B spermatogonia give rise to?

A

Primary spermatocytes.

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63
Q

What is spermiation?

A

The release of spermatids into the lumen of the seminiferous tubules.

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64
Q

How does sperm capacitation occur in in-vitro fertilisation?

A

The sperm must be incubated in a capacitation media.

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65
Q

What is the function of follicular cells?

A

To maintain and aid in the development of the primary oocytes.

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66
Q

What are primordial follicles?

A

Primary oocytes that are surrounded by follicular cells.

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67
Q

What do follicular cells metaplaise from and to in the preantral stage, and what is their new function?

A

They metaplaise from flat cells to stratified cuboidal cells, after proliferation, which are now called granulosa cells.
These secrete a layer of glycoprotein surrounded the oocyte, forming the zona pellucida.

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68
Q

What does a surge in luteinising hormone do?

A

Stimulates the preovulatary stage:
- Meiosis I completes forming a secondary oocyte (lots of cytoplasm) and a polar body (almost none).
- Meiosis II starts but arrests in metaphase.

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69
Q

When would meiosis II of the secondary oocyte complete, and what is formed from it?

A

If fertilisation occurs.
An ovum, when fertilised becomes a zygote, and a polar body.

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70
Q

Where do the 3 polar bodies come from?

A

The first polar body is from meiosis I.
The second polar body is from meiosis II.
The third polar body is from the division of the first polar body.

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71
Q

Why is prostaglandin synthesis increased during ovulation, and what does it cause?

A

It is increased as a result of an increase in luteinising hormone.
It causes muscular contractions in the ovarian wall.

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72
Q

What other cells are released with the oocyte in ovulation?

A

Cumulus oophorus.

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73
Q

If fertilisation occurs, what is the function of the corpus luteum?

A

To secrete oestrogens and progesterone.
Stimulates the uterine mucosa to enter the secretory stage for preparation of embryo implantation.

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74
Q

If fertilisation does not occur, what does the corpus luteum become?

A

The corpus albicans - a mass of fibrotic scar tissue.

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75
Q

What does the embryo release to prevent the degeneration of the corpus luteum?

A

Human chorionic gonadotropin.

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76
Q

What is the prostate formed from?

A

An outgrowth of urethral endoderm.

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77
Q

How does the broad ligament form?

A

Through the fusion of the paramesonephric ducts.

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78
Q

How does prostatic enlargement lead to incontinence?

A

Desensitisation of the stretch receptors in the bladder, due to an increase in urine retention.

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79
Q

Why does the external genitalia of a baby with the genotype 46,XX appear ambiguous?

A

The paramesonephric duct is present due to the absence of MIH.
The mesonephric duct (partially) develops, due to the presence of androgens.

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80
Q

Which cells of the anterior pituitary gland produce LH and FSH?

A

Gonadotropes.

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81
Q

What forms the hypophyseal portal system?

A

Primary capillary plexus.
Hypophyseal portal veins.
Secondary capillary plexus.

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82
Q

What is the pattern of GnRH release, after puberty?

A

Pulsatile, every 1-3 hours.

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83
Q

What does FSH stimulate in males, and what is the outcome?

A

Sertoli cells - spermatogenesis in the seminiferous tubules occurs. Inhibin is released.

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84
Q

What does LH stimulate in males, and what is the outcome?

A

Leydig cells - testosterone is released.

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85
Q

What does FSH stimulate in females, and what is the outcome?

A

Granulosa cells - follicular development and the formation of the zona pellucida. Inhibin also released.

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86
Q

What does LH stimulate in females, and what is the outcome?

A

Theca interna cells - androgen release, which is converted to oestrogen and progesterone.

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87
Q

What converts androgens into oestrogen and progesterone?

A

Granulosa cells.

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88
Q

How long after hormone secretions do physical signs of puberty show, roughly?

A

1 year.

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89
Q

What are the hormonal changes seen at the onset of puberty?

A

Increasing frequency and amplitude of GnRH secretions, which first occurs at night and then progressively throughout the day.
Steady increase in FSH and LH.

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90
Q

State the meaning of the following terms:
- Gonadarche
- Adrenarche
- Thelarche
- Menarche
- Pubarche.

A
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91
Q

State the rough order in which pubertal changes occur in males, and what they are.

A

Genital development - increased testicular size, and then increased penis size and scrotal changes.
Pubic hair growth.
Spermatogenesis.
Growth spurt.

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92
Q

What are the secondary sex characteristics of males?

A

Increased and thickened hair on the trunk, pubis, axillae and face.
Increased laryngeal size - adams apple.
Deepening of voice.
Increased bone mass.
Increased muscle mass and strength.

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93
Q

State the rough order in which pubertal changes occur in females, and what they are.

A

Thelarche - breast bud development.
Adrenarche - pubic hair growth.
Growth spurt.
Menarche - menstrual cycle begins.

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94
Q

What are the secondary sex characteristics of females?

A

Pubic and axillary hair.
Enlargement of the labia majora and minora.
Keratinisation of vaginal mucosa.
Uterine enlargement.
Increased fat in hips and thighs.

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95
Q

What is the growth spurt size dependent on, and why are males taller?

A

Depends on growth hormone, insulin-like growth factor 1 and sex steroids.
Males’ growth spurt occurs later, so epiphyseal growth plates fuse later, and their growth spurt is longer and slightly faster.

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96
Q

What causes female epiphyseal growth plate fusion?

A

Oestrogen.

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97
Q

What is the average menstrual cycle length?

A

28 days.

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98
Q

What are the 3 phases of the uterine cycle?

A

Menstrual.
Proliferative.
Secretory.

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99
Q

Which phase of the ovarian cycle is variable, and why is the other not?

A

Follicular phase is variable.
Lateral phase is not as the corpus luteum has a life span of 14 days, should fertilisation not occur.

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100
Q

What occurs in the early follicular phase, and how long is it?

A

Days 0 to 5.
No ovarian hormone production, initially, with granulosa cells secreting activin to increase FSH production. FSH receptors on granulosa cells increase.
This increased level of FSH then stimulates follicle growth and the theca interna formation, with secretion of oestrogen.
Inhibin is then released from the granulosa cells of the dominant follicle, preventing the development of any other follicles.

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101
Q

What occurs in the late follicular phase?

A

Oestrogen increases the FSH receptors on the follicle, and increases LH receptors on granulosa cells. It has a negative feedback on FSH production.
Inhibin helps LH to increase theca cell androgen production. Decrease FSH production.

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102
Q

What is the corpus luteum made from?

A

Granulosa and theca interna cells.

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103
Q

What is the outside of the uterus called?

A

Perimetrium - visceral peritoneum.

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104
Q

Outline the changes in the endometrium in the early proliferative, later proliferative and secretory phases.

A
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105
Q

What cells produce hCG?

A

Syncytiotrophoblasts.

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106
Q

What is precocious puberty, and what are the two types?

A

Puberty that occurs before the age of 9 in males, and 8 in females.
There is central (true) or peripheral (pseudo).

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107
Q

What is central precocious puberty?

A

Puberty that occurs before the age of 9 in males, and 8 in females.
Follows the normal pattern of puberty - breast bud development first in females and testicular growth in males.
It is due to GnRH rises.

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108
Q

What is peripheral precocious puberty?

A

Puberty that occurs before the age of 9 in males, and 8 in females.
It does not follow the normal pattern of puberty.
It is GnRH independent - oestrogen and/ or testosterone released early which cause early signs of puberty.

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109
Q

What is the most common first sign of peripheral precocious puberty?

A

Pubic or axillary hair growth.

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110
Q

What are the causes of precocious puberty?

A
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111
Q

How is central precocious puberty diagnosed?

A

GnRH stimulation test.
LH and FSH elevations.

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112
Q

What are some causes of peripheral precocious puberty?

A
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113
Q

How is peripheral precocious puberty diagnosed?

A

Increased oestrogen or testosterone levels in the blood.
Decreased LH and FSH due to negative feedback.

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114
Q

What is delayed puberty?

A

No pubertal changes before the age of 13 in females and 14 in males, or no developmental progression over a 2 year period.

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115
Q

What are some causes of delayed puberty?

A
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116
Q

What is hypogonadotrophic hypogonadism?

A

Where the hypothalamus or pituitary don’t stimulate the gonads, leading to low LH and FSH levels, and so no testosterone, or oestrogen and/or progesterone.

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117
Q

How can the cause of delayed puberty be determined?

A

Look at the BMI of the patient - check their nutritional intake. Could be the reason if BMI less than 18.
Karyotype for any chromosomal abnormalities.
Check for any chronic diseases.
Blood tests - LH, FSH and testosterone/ oestrogen.

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118
Q

What is hypergonadotrophic hypogonadism?

A

Where there is increased GnRH, FSH and LH, with low testosterone, or oestrogen and/or progesterone.
This is due to gonadal dysfunction.

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119
Q

A decrease in which hormone causes the corpus luteum to atrophy?

A

LH.

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120
Q

What is the issue with precocious puberty?

A

It will lead to short stature as fusion of the epiphyseal growth plates will occur sooner.

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121
Q

When does thelarche, adrenache, growth spurt and menarche occur in females?

A
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122
Q

What can be done to delay puberty, and what other help may the patient need?

A

Weight loss - decrease leptin.
Medroxiprogesterone to negatively feedback against GnRH, LH and FSH.
GnRH analogues in high doses to switch of the receptors.
Androgen blockers.
Therapy may be given to the patient.

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123
Q

What is primary amenorrhea?

A

The failure to establish menstruation by 15 years old with normal secondary sexual characteristics.
The failure to establish menstruation by 13 years old with no secondary sexual characteristics.

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124
Q

What is secondary amenorrhea?

A

Cessation of menstruation for 3-6 months in women with previously normal menses.
Cessation of menstruation for 6-12 months in women with previous oligomenorrhoea.

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125
Q

What are some causes of amenorrhea?
Hint: physiological, hypothalamic, pituitary, ovarian, uterine and vaginal.

A
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126
Q

What are some genitourinary malformations that can cause amenorrhea?

A

Imperforate hymen.
Vaginal septum.
Absent vagina.
Absent uterus.

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127
Q

What is an imperforate hymen, and how can it present?

A

Sinovaginal bulb fails to canalise, so the epithelium of the hymen remains.
It presents with amenorrhea as the blood cannot pass through, and can be painful, and appear as a bulge.

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128
Q

If there are no secondary sex characteristics, what does the cause of amenorrhea suggest?

A

An underlying chromosomal or hormonal cause.

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129
Q

Why can hypothyroidism cause amenorrhea?

A

Increased TRH secretions from the hypothalamus.
This increase prolactin secretions.
Prolactin inhibits GnRH secretions.

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130
Q

Why can hyperthyroidism cause amenorrhea?

A

Decreased free oestrogen.
This means there cannot be positive feedback on the anterior pituitary for LH secretions.
No LH surge for ovulation.

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131
Q

What is Asherman syndrome?

A

Adhesions and scarring in the uterus.
This prevents growth or shedding of the endometrium, leading to amenorrhea.

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132
Q

What is primary ovarian insufficiency?

A

Premature menopause, where there is depletion of oocytes before the age of 40.

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133
Q

What is the triad associated with polycystic ovarian syndrome?

A

Menstrual irregularity.
Androgen excess.
Obesity.

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134
Q

Why is PCOS associated with obesity?

A

There is increased insulin resistance, leading to increased adipose deposition.

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135
Q

How is PCOS diagnosed?

A

2 out of 3 of the following:

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136
Q

What are PCOS symptoms?

A

Hair loss.
Hirsutism.
Pelvic pain.
Weight gain.
Acne.
Irregular periods.
Infertility.

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137
Q

What is functional hypothalamic amenorrhea?

A

Weight loss and excessive exercise, or emotional or illness stress, causing cessation in periods.

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138
Q

What is oligomenorrhoea?

A

Infrequent menstruation with a cycle length between 6 weeks and 6 months.

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139
Q

What are causes of oligomenorrhoea?

A
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140
Q

How is menorrhagia diagnosed?

A

Menstrual blood loss of 80ml or more.
Duration of menstruation of more than 7 days.
The requirement of changing menstrual products 1-2 hourly.
Passage of clots or very heavy periods being reported by the woman.

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141
Q

What are some uterine and ovarian causes of menorrhagia?

A
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142
Q

Why does PCOS cause menorrhagia?

A

It prolongs the follicular phase.
This means there is an increase in size of the functional endometrial layers and so when it is shed, there is more bleeding.

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143
Q

What are some iatrogenic causes of menorrhagia?

A

Anticoagulant treatment.
Intrauterine contraceptive device.

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144
Q

What are some systemic diseases that can cause menorrhagia?

A

Coagulation disorders - Von willerbrand, factor V Leiden, etc.
Hypothyroidism.
Diabetes mellitus.
Hyperprolactinaemia.
Liver or renal disease.

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145
Q

What are uterine fibroids?

A

Leimyomas- benign tumours where there is proliferation of smooth muscle cells and fibroblasts, found within the myometrium.

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146
Q

What are risk factors for uterine fibroids?

A

Increasing age - until menopause where they regress (oestrogen).
Early menarche.
Older age at first pregnancy.
Black and Asian ethnicity.
Family history.

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147
Q

What is the first thing a doctor does when presented with a patient with menorrhagia?

A

Full blood count - often have anaemia.

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148
Q

What is the treatment for dysfunctional uterine bleeding?

A
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149
Q

What are some red flag signs for menorrhagia?

A

Post-menopausal bleeding.
Persistent inter-menstrual bleeding.
Persistent post-coital bleeding.
Pelvic mass/ bloating/ early satiety.
Ascites.

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150
Q

What is primary dysmenorrhea?

A

Painful cramping of the lower abdomen which occurs shortly before or during menstruation, or both - its onset is 6-12 months after menarche with no identifiable pelvic pathology.

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151
Q

What is the pathophysiology of primary dysmenorrhea?

A

Uterine prostaglandin production during menstruation causes the uterus to contract.

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152
Q

What is secondary dysmenorrhea?

A

Painful cramping in the lower abdomen, which occurs shortly before or during menstruation, or both, which starts several years after painless periods.

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153
Q

What are the causes of secondary dysmenorrhea?

A
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154
Q

What is the pathophysiology of endometriosis?

A

Ectopic endometrial gland and stroma outside the endometrial cavity, that produces oestrogen and leads to inflammation, fibrosis and scarring.
This is due to not all of the lining of the uterus being shed and some moving superiorly - retrograde menstruation.

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155
Q

Why can endometriosis be seen outside of the pelvis?

A

Because the female internal reproductive tract is continuous with the peritoneal cavity and so it can enter the peritoneal cavity.

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156
Q

How is endometriosis diagnosed?

A

Laparoscopy.

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157
Q

What are some common sites for endometriosis?

A

Fallopian tubes.
Rectum.
Bladder.

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158
Q

What are some risk factors for endometriosis?

A

Early menarche.
Late menopause.
Delayed childbearing.
Nulliparity - never given birth.
Family history.
Vaginal outflow obstruction - imperforate hymen.
White ethnicity.
Low BMI.
Autoimmune disease.
Late first sexual encounter.
Smoking.

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159
Q

What is adenomyosis?

A

Endometrial tissue found deep within the myometrium, causing heavy and painful periods.

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160
Q

What are some complications of endometriosis?

A

Deep pain during intercourse.
Painful bowel movements or urination during period.
Endometriomas - ovarian cysts contain blood and endometrial-like tissue.
Adhesions.
Bowel obstructions.
Chronic pain.
Reduced quality of life.
Infertility due to scarring in the fallopian tube.
Ovarian cancer.

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161
Q

What is the management of primary dysmenorrhea?

A

NSAIDs or paracetamol.
Oral contraceptive trials of 3-6 months - combined oral contraceptive pill, or progesterone oral pill.
Conservative advice.

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162
Q

What is the management of secondary dysmenorrhea, caused my endometriosis?

A
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163
Q

Define the terms:
- Menopause.
- Perimenopause.
- Menopause transition.
- Early menopause.
- Premature menopause.
- Surgical menopause.

A
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164
Q

What is pathological menopause?

A

The cessation of menstruation before the age of 40.

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165
Q

What is the period regularity, hormonal and age appearance of a pre-menopausal woman?

A

Regular periods with some symptoms experienced.
Slight elevations to FSH/ LH levels, with a low oestrogen.
Typically above the age of 40 with decreased fertility.

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166
Q

What is the peri-menopause characterised by?

A

Physiological changes decreasing the reproductive capacity with abnormal ovulations due to a decrease in follicle number.

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167
Q

Why does the quality of the oocytes change as a woman ages?

A

The oocytes have been arrested in meiosis I for longer, increasing the risk of abnormalities for any potential children.

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168
Q

When is FSH test used to diagnose menopause?
How?

A

Women aged 40-45 with menopausal symptoms.
Women under the age of 40 - primary ovarian insufficiency - 2 blood samples taken 4-6 weeks apart.

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169
Q

What are vasomotor symptoms due to?

A

Decreased oestrogen levels.

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170
Q

State some symptoms of menopause.

A
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171
Q

What are some dysfunctional uterine bleedings?
What are they often caused by?

A

Intermentrual bleeding - between periods.
Heavy bleeding.
Mid-cycle bleeding.
Irregular cycles.

Often caused by changes in oestrogen.

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172
Q

What are psychological changes seen in menopausal women?

A

Irritability.
Confusion.
Lethargy.
Memory loss.
Loss of libido.
Depression.

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173
Q

What are anatomical changes seen in the GI and urinary tracts due to menopause?

A

GI - motor activity diminished.
Urinary - drying, thinning and decreased elasticity of the bladder, and the lining of the urethra.

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174
Q

What are some symptoms seen in the urinary system, due to menopause?

A

Loss of pelvic tone.
Urinary incontinence.
Urinary urgency, nocturia and dysuria.
Increased risk of UTIs.

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175
Q

Why is there an increased risk of UTIs in post-menopausal women?
How is this prevented?

A

The absence of oestrogen decreases the vaginal glycogen stores meaning lactobacillus decreases in number and function, increasing the pH from 4.0 to 7.0.

It is prevented by treating with topical oestrogens.

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176
Q

What are some genital organ changes in post-menopausal women?

A

Thinning of the vaginal skin - can cause superficial dyspareunia and bleeding.
Regression of the endometrium.
Shrinkage of myometrium.
Thinning of the cervix.

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177
Q

Why do breasts sag after menopause?

A

Low oestrogen levels decreases the elasticity of the connective tissue.

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178
Q

What contraceptive advice should be given to menopausal women?

A

Contraception is needed until periods have stopped for 1 year if over 50, if under 50 then they need to have stopped for 2 years.
This is because peri-menopausal women can still get pregnant.

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179
Q

What are the benefits of HRT?

A

Reduction in vasomotor symptoms.
Improvement in mood changes.
Improvement in urogenital symptoms.
Reduction in osteoporosis risk.
Lower risk of colorectal cancer.
Maintenance of muscle mass and strength, and connective tissue.

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180
Q

Which HRT increases the risk of endometrial and breast cancer?

A

Oestrogen-only HRT.

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181
Q

What is the drawback of oral HRT?

A

Increased risk of venous thrombo-embolism.

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182
Q

Outline the advantages and disadvantages of oral, transdermal, vaginal and mirena intrauterine device HRT.

A
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183
Q

What is PCOS associated with (cause)?

A

A lack of pulsatile GnRH.

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184
Q

What is metrorrhagia?

A

Irregular periods.

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185
Q

What are the functions of seminal plasma?

A

Acts as a transport medium for sperm.
Gives nutritional support to sperm.
Acts as a pH buffering capacity for vaginal pH.
Contains prostaglandins which stimulate muscular activity within the female tract.

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186
Q

What is tested for in semen analysis?

A
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187
Q

What is the refractory period in the male sex response?

A

The time between the male can next orgasm - can be minutes to days.

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188
Q

How does the blood in a flaccid penis run?

A

Arterio-venous anastomoses allows blood to bypass the corpus cavernosum.

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189
Q

What changes are seen in blood vessels for an erection to occur?

A

The smooth muscle of the helicine arteries relax and straighten.

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190
Q

Which muscles of the pelvic floor compress the venous plexus during erection?

A

Blubospongiosus and ischiocavernosus.

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191
Q

State some causes of erectile dysfunction.

A
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192
Q

What is ejaculatory expulsion?

A

The expulsion of semen through the urethra, out the external urethral meatus.

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193
Q

During the menstrual cycle, how does the cervical mucus change?

A

Follicular phase - thick mucus.
Ovulation - watery mucus.
Lateral phase - thick mucus.

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194
Q

What occurs in the 4 phases of the female sexual response?

A

Excitement - clitoral enlargement, swelling of the labia and vaginal lubrication is formed.
Plateau - uterus elevates, labia change colour and the vagina expands (tenting). The orgasmic platform forms.
Orgasm - uterine contractions, rhythmic contractions of the vagina and anal sphincter contractions.
Resolution - seminal pool forms, the vagina returns to normal and the orgasmic platform disappears.

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195
Q

What is the acrosome?

A

Part of the head of the sperm, derived from the golgi region of the spermatid, containing enzymes.

196
Q

What occurs in the acrosome reactions?

A

Sperm pushes through the corona radiata (outer granulosa cells).
Binding of sperm surface receptor of the zona pellucida.
Acrosome reaction occurs.
Digestion of the zona pellucida.

197
Q

What occurs in fertilisation?

A

Fusion of the plasma membranes from the sperm and secondary oocyte.
Cortical reaction occurs - prevents polyspermy.
Meiosis II is completed.
Pronuclei move together.
Mitotic spindle forms, leading to cleavage.

198
Q

What is physiological discharge?

A

Discharge in females that is white or clear and non-offensive, that changes with the menstrual cycle.

199
Q

How does the discharge change throughout the ovarian cycle?

A

Follicular phase - small volumes of thick cervical mucus.
Ovulation - abundant and elastic cervical mucus.
Luteal - small volumes of thick cervical mucus.

200
Q

How is vaginal candidiasis treated?

A

Fluclonazole - tablet.
Clotrimazole - topical.

201
Q

What are risk factors for bacterial vaginosis?

A

Sexual activity.
Receiving oral sex.
Vaginal washes/ douches.
Smoking.

202
Q

What can be seen in a gram stain of bacterial vaginosis?

A

Clue cells.

203
Q

What is bacterial vaginosis?

A

An overgrowth of anaerobic bacteria, such as gardnerella vaginalis.

204
Q

How is bacterial vaginosis treated?

A

Metronidazole orally.
Clindamycin gel.

205
Q

What kind of bacteria is chlamydia trachomatis, and what is its virulence factor?

A

Obligate intracellular bacterium, with a unique cell wall that inhibits phagolysosome fusion.

206
Q

Describe the bacteria that cause gonorrhoea?

A

Neisseria gonorrhoea:
- Gram negative.
- Diplococci.
- Unencapsulated.

207
Q

What are high-vaginal swabs testing for?

A

Trichomonas.
Candida.
Bacterial vaginosis.

208
Q

What are endocervical swabs testing for?

A

Chlamydia.
Gonorrhoea.

209
Q

What are vulvovaginal (self) swabs testing for?

A

Chlamydia.
Gonorrhoea.

210
Q

What kind of virus is HPV, and what does it cause?

A

Non-enveloped DNA virus.
It causes genital warts, and can increase the risk of cervical cancer.

211
Q

What are the two HPV vaccines, and what do they give immunity against?

A

Gardasil - strains 6, 11, 16, and 18.
Cervarix - strains 16 and 18.

212
Q

How is HPV treated?

A

Complex treatment.
Can give antivirals.
Can freeze the warts off.

213
Q

What kind of virus are the herpes simplex viruses?

A

Enveloped DNA viruses.

214
Q

What type of bacteria causes syphilis?

A

Treponema pallidum - a spirochete.

215
Q

What types of infections are encompassed by the term pelvic inflammatory disease?

A

Endometritis.
Salpingitis - fallopian tubes.
Parametritis - pelvic floor fascia.
Oophoritis - ovarian infections.
Tubo-ovarian abscess.
Pelvic peritonitis.

216
Q

What are some symptoms of pelvic inflammatory disease?

A
217
Q

What are some clinical signs of PID?

A
218
Q

What are some PID complications?
Early and late.

A

Early - sepsis and peritonitis.

Late:
- Chronic pelvic pain.
- Pelvic abscess.
- Infertility.
- Ectopic pregnancy.
- Fitz-Hugh Curtis syndrome.

219
Q

How is PID managed?

A

Empirical antibiotics - ofloxacin and metronidazole.
Screen for other STIs.
Contact tracing.
Advise.

220
Q

What additional samples should be done for men who have sex with men?

A

Rectal and pharyngeal sampling.

221
Q

If the menstrual cycle of a woman is 35 days, when should the progesterone be measured to see if ovulation has occurred?

A

Day 28 of the cycle.
It should always be 7 days before the next period.

222
Q

Why is it useful to measure the body temperature daily for menstruating women, and why does it need to be taken at the same time every day?

A

It can show that ovulation has occurred because an increase in progesterone increases the body temperature.
Temperature varies throughout the day due to the circadian rhythm.

223
Q

How long perviously does ovulation occur, from the last menstrual cycle, and why?

A

14 days - the corpus luteum always lasts for 14 days.

224
Q

What are the 2 most common causes of secondary amenorrhoea and what hormones can be used to test for them?

A

Pregnancy - hCG.
Weight loss - GnRH.

225
Q

What are the disadvantages of abstinence and withdrawal contraception?

A

Abstinence - not an option for most and unprepared if they become sexually active.

Withdrawal - unreliable, some sperm in the pre-ejactulate and no STI protection.

226
Q

What does fertility awareness methods monitor, and why would somebody use it?

A

Looking at cervical secretions - become more stretchy and thinner when fertile, and changes to the cervix.
Basal body temperature - increases after ovulation due to increasing progesterone levels released from the corpus luteum.
Tracking the periods via calendar.

It is natural - there are no hormones or barriers involved, and it may be particularly suitable for certain religions.

227
Q

For how long can lactational amenorrhoea contraceptive be effective for?

A

Up to 6 month postnatally.

228
Q

What kind of contraception may be advised for a sex female worker?

A

Female condoms - prevent pregnancy and STI contractions.

229
Q

What are the advantages of the combined oral contraceptive pill?

A

Reliable contraception method.
Can relieve menstrual disorders by thinning the endometrium.
Decreases the risk of ovarian cancer, by decreasing ovulations, and endometrial cancer by thinning the endometrium.
Decreases acne severity in some.

230
Q

Who can the COCP not be used for?

A

It cannot be used for people who have; raised BMI, migraines and aura (visual disturbances), breast cancer (previously had) and those that smoke.

231
Q

What are the disadvantages of the COCP?

A

User dependent - taking it every day.
No STI protection.
Can interact with other medications.
Cannot be used for everyone.
Side effects - menstrual irregularities, breast tenderness, and mood disturbances.
Increased risk of CV disease, venous thromboembolism, stroke, breast and cervical cancer.

232
Q

Why can the progesterone only pill increase the risk of ectopic pregnancies?

A

Reduced activity of cilia. So zygote does not move from the site of fertilisation well.

233
Q

How long can fertilisation take to return after the progesterone injection?

A

18 months.

234
Q

What are the advantages and disadvantages of the progesterone implant?

A

Advantages:
- Reliable.
- Can last up to 3 years.
- Can be used instead of the COCP if contraindicated.
- Fertility returns faster than with injections.

Disadvantages:
- No STI protection.
- Menstrual irregularities.
- Complications with inserting and removing the implant.

235
Q

What contraceptive can be used as treatment for menorrhagia?

A

Intrauterine system.

236
Q

How long must a man wait for unprotected sex after a vasectomy?

A

12 weeks.

237
Q

What is the ‘morning after pill’ and how does it work?

A

Levonorgestrel.
A high dose progesterone pill that inhibits ovulation. It can be taken up to 72 hours after unprotected sexual intercourse.

It is only effective if the woman has not ovulated yet.

238
Q

What is ulipristal acetate, and how does it work?

A

A selective progesterone receptor modulator, that prevents the LH surge, stopping or delaying ovulation.
It works up to 120 hours post unprotected sexual intercourse.

239
Q

Define subfertility.

A

Reduced fertility that results in a prolonged duration of unwanted lack of conception.

240
Q

What is the conception percentages for 1, 2 and 3 years of regular unprotected coitus?

A

1 year - 84%.
2 years - 92%.
3 years - 93%.

241
Q

What are, and what are some examples of, pre-testicular causes of male infertility?

A

Disorders of the hypothalamus and pituitary that stop sperm production.

Hypogonadotrophic hypogonadism.
Thyroid disorders.

242
Q

What are, and what are some examples of, testicular causes of male infertility?

A

Defective production of sperm.

Genetic - Kleinfelters syndrome (XXY) where the testes do not descend.
Congenital - cryptochidism: an absence of a testicle.
Infective - mumps.
Antispermatogenic agents - chemotherapy.
Vascular - torsion and varicocele.

243
Q

What are, and what are some examples of, post-testicular causes of male infertility?

A

Obstruction or sexual problems that prevent the delivery of sperm to the oocyte.

Obstructive - CBAVD (absent vas deferens), infections causing scarring, or vasectomy.
Coital - sexual dysfunction or hypospadias (urethral opening lower down).

244
Q

What male examinations for fertility would be performed?

A

Penile examinations for structural abnormalities.
Scrotal examination.
Secondary sexual characteristic examination.

245
Q

What are the two derivatives of the placenta?

A

Fetal part - chorionic sac.
Maternal part - endometrium.

246
Q

What are decidual cells dervied from, and what are their functions?

A

Stromal cells.

Highly specialised secretory epitheloid cells that control the depth of trophoblast invasion and protect the concepts from maternal immune rejection.

247
Q

Why may the zygote be rejected by the mother?

A

It is 50% foreign, with the genetic material coming from the father.

248
Q

What is the normal depth of invasion of the zygote?

A

Stratum functionalis - decidual layer.

249
Q

How does implantation attachment occur?

A

Weakly - trophoblastic microvilli binds to pinopodes.

Strongly - trophoectoderm integrins bind to endometrial integrin receptors to form strong bonds.

250
Q

What are between the syncytiotrophoblast roots?

A

Lacunae, which fill with maternal blood.

251
Q

How do the syncitiotrophoblasts invade the endometrium?

A

They produce enzymes that can break down the stroma.
The enzymes can also break down the blood vessels to fill the lacunae with blood.

252
Q

What is the primary villus?

A

Projections of cytotrophoblasts that enter the syncytiotrophoblasts.
There are intervillus spaces that can be filled with blood.
They form a cytotrophoblastic shell at day 13-15.

253
Q

What becomes the umbilical cord?

A

The connecting stalk - the umbilical vessels are contained within.

254
Q

Where is the extraembryonic mesoderm found between on day 12 post-fertilisation, and what is it divided into?

A

The cytotrophoblasts and embryoblasts.
It is divided into splanchnic and somatic mesoderm.

255
Q

What is the space between the splanchnic and somatic mesoderm?

A

Chorionic cavity.

256
Q

What is the secondary villus, when is it formed and what else happens during when this forms?

A

The somatic extraembryonic mesoderm invades into the primary villus.
It occurs between days 16 and 21.

The connecting stalk differentiates to form the two umbilical arteries and the umbilical vein.

257
Q

What happens to form the tertiary villus and when does this occur?

A

The chorionic vessels grow up into the villus, which are branches of the umbilical vein and artery.
This occurs between day 17 and 22.

258
Q

What are cotyledons?

A

They are septae formed from decidua which separate the tertiary villi into groups, around the 4th-5th month.

259
Q

Why is there gross haemorrhage with ectopic pregnancies?

A

The depth of the invasion is not controlled by decidual cells and so they invade into the vessels.

260
Q

What kind of haemorrhage occurs with placenta praevia?

A

Ante-partum haemorrhage.

261
Q

What are the 3 types of too-deep implantations?

A

Placenta accreta - into the stratum basalis.
Placenta increta - into the myometrium.
Placenta percreta - invasion through the uterus.

262
Q

What can be the issue of too deep implantation?

A

During labour, the placenta does not detach easily and so post-partum haemorrhage can occur.

263
Q

What are the different types of placenta praevia?

A
264
Q

What are the transfer functions of the placenta?

A

Gas exchange.
Nutrient exchange.
Removal of waste.
Immunity.

265
Q

What are the protein hormones released from the placenta?

A

Human chorionic gonadotrophin.
Human placental lactogen.
Placental growth hormone.
Corticotropin-releasing hormone.

266
Q

What two trophoblast diseases can see an increased hCG?
Describe them.

A

Molar pregnancy - incorrect chromosome number; compete = only paternal chromosomes, partial = extra set of chromosomes.
Choriocarcinoma - cancer of the chorion.

267
Q

What can an inadequate uteroplacental circulation cause?

A

Fetal distress.

268
Q

What is the transfer of passive immunity and how long does this last for?

A

Receptor-mediated endocytosis of IgG.
It lasts for 6 months.

269
Q

What therapeutic drugs can pass through the placenta?

A

Anti-epileptic drugs - sodium valproate can cause neural-tube defects.
Warfarin.
ACE inhibitors.

Thialomide (anti-morning sickness) - limb defects.

270
Q

What are some infections that can pass through the placenta?

A
271
Q

What condition can cause a false-positive pregnancy test, and why?

A

Hyperthyroidism as the excess hormones can mimic the hCG hormone.

272
Q

What anatomical landmark gives an estimate for the symphysis-fundal height at 20 weeks?

A

Umbilicus.

273
Q

Why is oligohydraminos associated with compromise of the uteroplacental circulation?

A

Placental hypoperfusion means that there is insufficient blood supply to the fetus, which leads to the fetus prioritising the brain and heart, decreasing the blood flow to the kidney.

274
Q

Prior to week 10, how is amniotic fluid produced?

A

Transudation across the skin of the fetus.

275
Q

How might the uteroplacental or fetoplacental circulations be investigated?

A

Doppler ultrasound.

276
Q

What are two causes of adhesions?

A

Inflammation.
Surgery.

277
Q

Why is scalp electrode monitoring of the fetus used?

A

To monitor the fetal heart rate consitnuously, for better accuracy.

278
Q

Why may smoking during pregnancy affect oxygen flow to the fetus?

A

Smoking contains carbon monoxide. This increases the R-state of the haemoglobin, for oxygen. This means that the mother gives up oxygen less readily to the fetus.
Atherosclerotic changes to the maternal arteries can decrease the supply of blood to the placenta.

279
Q

What are some signs of fetal distress?

A

Presence of meconium.
Fetal bradycardia.
Decreased movement of the fetus.
Bleeding.
Oligohydraminos.

280
Q

Which developmental period is the organogenetic period?
Why?

A

The embryonic period - characterised by intense activity for development of the rudimentary organ systems.

281
Q

When do symmetrical, asymmetrical and mixed growth restrictions occur?

A

Symmetrical = 0-20 weeks.
Mixed = 20-28 weeks.
Asymmetrical = 28-40 weeks.

282
Q

At birth, what proportion of the baby is the length of the head?

A

1/4-1/3rd.

283
Q

What is a normal symphysis fundal height measurement?

A

The number of weeks pregnant +/- 2cm.

284
Q

What type of scan is the 12 week scan, and what can it look for?

A

Transabdominal, dating scan.

It determines gestational age - dating the pregnancy, via the crown-rump length.
Can detect multiple pregnancies.
Screening for chromosomal abnormalities via the nuchal translucency scan.

285
Q

What type of scan is the 20 week scan, and what can it look for?

A

Transabdominal, anomaly scan.

Screen for fetal abnormalities, looking at the body systems for structural abnormalities.
Determine the placental location.
The sex of the fetus.

286
Q

What is the bipartietal diameter, when is it used and what is it used with?

A

Measuring the diameter of the parietal bones of the fetal skull.

It is used in the 2nd and 3rd trimesters.

It is used in combination with abdominal circumference and femur length, to help detect anomalies.

287
Q

What are the weight classifications of a baby who has macrosomia, a normal birth weight, a low, very low and extremely low birth weight?

A

Macrosomia = >4kg.
Normal = 3.5kg.
Low = <2.5kg.
Very low = 1.5-1kg.
Extremely low = <1kg.

288
Q

How can symmetrical intrauterine growth restriction be diagnosed prenatally, and what can this be due to?

A

Abdominal circumference, biparietal diameter and femur length all proportionally reduced.

Can be caused by genetic disorders or TORCH infections.

289
Q

How can asymmetrical intrauterine growth restriction be diagnosed prenatally, and what can this be due to?

A

Abdominal circumference is decreased, with the biparietal diameter and femur length normal.
The brain is still developing and so gets most of the nutrition, decreasing the nutrition to other parts of the body.

Placental insufficiency, such as in pre-eclampsia.

290
Q

When is the embryonic stage of lung developement and what happens in it?

A

Weeks 0-7.

The respiratory diverticula outpouches from the forgut, and forms the tracheooesophageal septum.
The trachea, left and right main bonrchi, and the segmental bronchi are formed.

291
Q

When is the pseudoglandular stage and what happens in it?

A

Weeks 7-16.

The duct system of the bronchopulmonary segments, created during the embryonic period, begins to form, forming the terminal bronchioles.

292
Q

When is the canaliculi stage and what happens in it?

A

Weeks 16-27.

Budding from the bronchioles formed in the psuedoglandular stage, forms the respiratory bronchioles.
Differentiation of some cuboidal cells to type I and II pneumocytes.

NOTE: some gas exchange possible towards the end of this stage.

293
Q

When is the saccular stage and what happens in it?
Why is this stage so important?

A

Weeks 24-36.

Terminal sacs begin to bud from the respiratory bronchioles.
Differentiation of type I and II pneumocytes is rapid.
It is so important because surfactant is now beginning to be produced (week 24), and so the fetus can be viable.

294
Q

When is the alveolar stage and what happens in it?

A

36+ weeks.

Mature alveoli form due to septation between the alveolar spaces.
Proliferation and expansion of capillaries, nerves and gas exchange areas.

295
Q

At what age are the lungs fully mature?

A

8 years old.

296
Q

How is respiratory distress syndrome managed, antenatally and neonatally?

A

Antnatally - 2 doses of glucocorticoid treatment to the mother to increase surfactant production of the fetus before delivery.

Neonatally:
- Nasal continuous positive airway pressure, forcing oxygen in to keep them open (nCPAP).
- Surfactant replacement therapy, in liquid form.
- Mechanical ventilation.

297
Q

When is the first heart beat?

A

From 5-6th week.

298
Q

At the 8 weeks transvaginal ultrasound, what is looked for?

A

Ectopic pregnancies.
Heart beat.

299
Q

What are some causes of oligohydraminos?

A
300
Q

What are some causes of polyhydraminos?

A

Oesophageal atresia or anencephaly.
Gestation diabetes - increases urine production.
Fetal anaemia.
Multiple pregnancies.

301
Q

What are the corticospinal tracts required for, and when do they start to develop?

A

Coordinated voluntary movements.
They start to develop from the 4th month.

302
Q

When does myelination of the brain begin?

A

9th month of pregnancy.

303
Q

When does the first movements of the fetus occur, and what kinds of movements are they?

A

Around the 8th week.
These are more reflexive responses, as they do not have the voluntary movements yet (corticospinal tract development needed).

304
Q

What is quickening?

A

The maternal awareness of the fetal movements from weeks 15-17 onwards.

305
Q

What are infants born pre-term at risk of, and what can be given to prevent some of these?

A

Neurodevelopmental disorders, such as cerebral palsy.
Hypoxia due to a decreased lung function - RDS.
Interventricular haemorrhage due to the brain’s blood vessels being poorly developed.

Magnesium sulphate - fetal neuroprotection given between 24 and 29 weeks gestation.

306
Q

At what weeks do the following occur?
- Cerebellar development.
- Myelination of the spinal cord starting.
- Gyri and sulci appearing.

A

CD - 16 weeks.

Myelination of SC - 20 weeks.

G&S - 28 weeks.

307
Q

What constitutes the maternal-fetal exchange?

A
308
Q

What facilitates the movement of oxygen from the maternal to fetal red cells?

A

Partial pressure differences - 4kPa in fetus to 11-13kPa from mother.
Fetal haemoglobin - higher affinity for oxygen.
Double Bohr and double Haldane effect.

309
Q

What is the fetal haemoglobin formed from and why does it have a greater affinity for oxygen than adult haemoglobin?

A

HbF - 2 alpha and 2 gamma subunits.
Greater affinity because it doesn’t bind 2,3-BPG as effectively as HbA.

310
Q

What is the double Haldane effect?

A

As maternal RBCs give up oxygen, it increases its affinity for carbon dioxide.
As fetal RBCs give up carbon dioxide, it increases its affinity for oxygen.

311
Q

What does the ductus venous connect?
Why?

A

The umbilical vein carrying deoxygenated blood to the inferior vena cava, ensuring blood enters the right atrium.
This prevents the liver from dropping the saturation of oxygen too low, it drops from 70% to 65%.

312
Q

What is the response of the of the fetus to hypoxia?

A

Fetal chemoreceptors detect the decrease in partial pressure of oxygen or increased partial pressure of carbon dioxide.
They then stimulate the vagus nerve to decrease the heart rate, causing bradycardia.
This decreases the demand for oxygen, of the heart.

There is also redistribution of blood flow to the heart and brain, reducing blood supply to the GI tract, kidneys and limbs.

313
Q

What is the outcome of chronic hypoxaemia?

A

Growth restriction.
Reduced fetal movement.

314
Q

Where is amniotic fluid reabsorbed?

A

Fetal GI tract when they swallow the amniotic fluid.
Placenta and fetal membranes - intramembranous.

315
Q

What is the composition of amniotic fluid?

A
316
Q

What is the meconium?

A

Debris from the amniotic fluid accumulating in the gut of the fetus and intestinal secretions, such as bile, forming a black tar-y stool.

317
Q

What is intrapartum monitoring, and how is it performed?

A

Monitoring the fetus during labour.

Intermittent auscultation:
- Listening to the heart rate for one minute using a Doppler every 15 minutes during the first stage.
- Listening for 1 minute, every 5 minutes furing the second stage of labour (when the baby is being delivered).

318
Q

What is CTG and how is it interpreted?

A

Cardiotogoraphy - continuous monitoring, looking at uterine contractions and the heart rate of the fetus in high risk pregnancies.

319
Q

What causes a small amount of blood to enter the right ventricle?

A

The crista dividens, preventing atrophy of the right ventricle.

320
Q

What is the cause of an increased fetal heart rate?

A

Increased fetal movement.

321
Q

What is cholestasis of pregnancy?

A

Intra-hepatic cholestasis of pregnancy can occur due to a decrease in contractions of the gallbladder, resulting most commonly in pruritis.

322
Q

What stimulates appetite and deposition of fat within the first trimester of pregnancy, and what benefit is this?

A

Progesterone.

Builds up stores for fatty acid use in the second and third trimesters, allowing the fetus to use the plasma glucose.
Breast growth.

323
Q

What anatomical affect does the expanding uterus have on the respiratory system of the mother?

A

The uterus pushes up against the diaphragm, decreasing the residual volume and total lung capacity.
Widening of the costal angle, expanding the rib cage, to increase the tidal volume.

324
Q

What are fetal decelerations?

A

Decrease in fetal heart rate.

325
Q

Why are pregnant women encouraged to lie on their left?

A

To prevent the compression of the inferior vena cava.

326
Q

What are the tendon reflexes like in a pre-eclampsia pregnant woman?

A

Hyper-reflexiveness due to an overactive CNS through vasospasms of the cerebral vessels, due to an increased intracranial pressure.

327
Q

How does magnesium sulphate work to treat eclampsia?

A

Vasodilation decreases the blood pressure in the cerebral vessels, preventing vasospasm.

328
Q

What does a hemi-allograft mean?

A

Where the fetus is formed from half of foreign material to the mother - 50% from the father.

329
Q

What hormone causes an immunosuppressed state in the pregnant mother, and what is the result of this?

A

Placental progesterone - changes the cytokine balance.

Higher attack rate of certain viral pathogens.
Improvements of certain autoimmune conditions.

330
Q

What is the effect of progesterone on the respiratory system of a pregnant woman?

A

Increased sensitivity of the respiratory centres for carbon dioxide, causing hyperventilation.
Bronchodilator effects.

331
Q

What are the changes in tidal volume, minute ventilation, expiratory reserve volume, total lung capacity and pH, during pregnancy?

A

Tidal volume - 30-40% increase.
Minute volume - 40-50% increase.
Expiratory reserve volume - 20% decrease.
Total lung capacity - 5% decrease.
pH - respiratory alkalosis, compensated by the kidney.

332
Q

How frequent is dyspnoea of pregnancy and why does it occur?

A

60-70% of patients.

Multifactorial.
Increased wakefulness drive.

333
Q

What are the consequences of changes within the CVS of a pregnant woman?

A

Increased RAAS (through increased oestrogen and progesterone) can lead to peripheral oedema, through increased fluid reabsorption.

Dilutional anaemia a greater increase in the fluid compartment of the blood than red cell production increase.

Increased risk of DVT and PE due to hypercoagulability.

334
Q

How much does the red cell mass increase by in pregnancy, and what is the most common cause of pregnancy anaemia?

A

25-30%.

Iron-deficiency anaemia, despite the general macrocytosis of cells within the pregnant body.

335
Q

What are the different parameters of anaemia in pregnancy?

A

1st trimester - Hb less than 110g/L.
2nd trimester - Hb less than 105g/L.
3rd trimester - Hb less than 100g/L.

336
Q

What are the complications of anaemia in pregnancy?

A

Increased morbidity for mum and baby due to the decreased oxygen carrying capacity.
Pre-term delivery.
Maternal fatigue.
Infant iron deficiency anaemia.

337
Q

Why can some liver function tests not be valid in pregnancy?

A

ALP levels increase due to placental synthesis.

338
Q

What can the effect of progesterone be on the lower oesophageal sphincter?

A

Decreases the tone of it, causing GORD and aspiration.

339
Q

What is the effect of pregnancy on phosphate levels, and why?

A

Increased excretion, decreases plasma levels.
The placenta releases PTH-related proteins.

340
Q

What are the risk factors for gestational diabetes?

A
341
Q

How is gestational diabetes diagnosed?

A

Oral glucose tolerance test.

Fasting plasma glucose of 5.6mmol/L or above.
A 2-hour plasma glucose level of 7.8mmol/L or above.

342
Q

What are the complications of gestational diabetes on the mother?

A

Increased risk of:
- Pre-eclampsia.
- Polyhdraminos (diabetes state).
- Premature labour.

Shoulder dystocia.
Failure to progress during pregnancy.

Increased risk of type 2 diabetes mellitus.

343
Q

What are the complications of gestational diabetes on the baby?

A

Macrosomia.
Hypoxia.
Sudden intrauterine death after 36 weeks gestation.
Cardiac, renal and neural tube defects.

Neonate:
- Hypoglycaemia.
- Respiratory distress.
- Jaundice.

344
Q

What are the MSK symptoms of pregnancy?

A

Back and shoulder pain.
Tension headaches.
Pelvic pain.
Carpal tunnel syndrome.

345
Q

What increases the motility of the sacroiliac joints and pubic symphysis in pregnancy?

A

Increased relaxin and progesterone hormones.

346
Q

How is pre-eclampsia defined?

A

A new onset of hypertension of >140/90 after 20 weeks gestation with 1 or more of:
- Proteinuria.
- Maternal organ dysfunction.
- Uteroplacental dysfunction.

347
Q

What is severe pre-eclampsia?

A

Pre-eclampsia with severe hypertension that does not respond to treatment.

348
Q

What are the risk factors for pre-eclampsia?

A
349
Q

What causes the impaired invasion of trophoblasts in pre-eclampsia?

A

Abnormal decidualisation.

350
Q

What are the symptoms of pre-eclampsia?

A

Headache.
Vision disturbance - blurring/ flashing.
Epigastric pain.
Swelling of the hands, feet or face.
Vomiting.
Shortness of breath.

351
Q

Why can a pulmonary embolism be hard to rule out in pregnancy?

A

The D-dimers are always raised.

352
Q

What are the complications of pre-eclampsia for the mother?

A

Eclampsia.
Cerebral haemorrhage.
Renal failure.
Pulmonary oedema.
DIC.
HELLP syndrome.

353
Q

What is HELLP syndrome?

A

Haemolysis.
Elevated liver enzymes.
Low platelets.

354
Q

What are the complications of pre-eclampsia on the fetus?

A

Asymmetrical growth restriction.
Oligohydraminos.
Placental infarct or abruption.
Fetal distress.
Premature delivery.
Stillbirth.

355
Q

What are the, and the normal time lengths for the first, second and third stage of labour?

A

First = onset of established labour - regular uterine contractions - until cervical dilation of 10cm. 14 hours.
Second = full dilation until the fetus is born. 1-2 hours.
Third = from the birth of the fetus until delivery of the placenta and membranes. 30 minutes.

356
Q

How is the birth canal formed?

A

Softening of the pelvic ligaments allowing some expansion to occur.
Increased myometrium activity for contractions.
Cervical dilation and effacement.

357
Q

What is cervical ripening?

A

The release of prostaglandins E2 and F2a, causing:
- Increased synthesis of glycosaminoglycans.
- Decreased synthesis of collagen.
- Decreased aggregation of collagen fibres and loosening of collagen bundles.
- Influx of inflammatory cells, increased NO output.

358
Q

What are the different contractions of the myometrium and how are these influenced?

A

Early pregnancy - low amplitude, ever 30 minutes that cannot be felt.
Brixton-Hicks - later on that are noticeable, but have a reduced frequency but increased amplitude.

Prostaglandins increase the release of Ca2+ intracellular stores.
Oxytocin lowers the threshold for triggering action potentials.

359
Q

What kind of hormone is oxytocin?

A

Peptide.

360
Q

State the 7 phases of the second stage of labour.

A
361
Q

Why are the placental membranes checked?

A

To ensure there is no postpartum haemorrhage, if any is left in the uterus.
To ensure it is not incomplete and has undergone infarction.

362
Q

What is the physiological 3rd stage of pregnancy?

A

No medication is used.
Midwife waits until the umbilical cord stops pulsating before cutting it.
Delivery of the placenta occurs passively.

363
Q

What is the active 3rd stage of pregnancy?

A

Oxytocin or ergometrine injections are given stimulating the uterus to contract, releasing the placenta.
The blood supply is reduced by closing the blood vessels, decreasing haemorrhage.

364
Q

What is the apgar score?

A
365
Q

What are the 4 different types of female bony pelvis and which is the common?
State the diameter of the most common one.

A

Gynecoid - most common and is 11cm.

Android.
Anthropoid.
Platypelloid.
The latter 3 are smaller.

366
Q

How can the fetus adapt shape for labour?

A

Molding:
- Fetal head changes shape from external compressive forces though the overlap of sutures.
- Diameter is reduced.

367
Q

What is fetal lie and what are the 3 types?

A

The relation of the long axis of the fetus to that of the mother.

Longitudinal - 99%.
Transverse - if not, a turn then a caesarean must be performed.
Oblique - unstable.

368
Q

What is the issue with a breech pregnancy?

A

The head is the largest diameter of the fetus.
This means that if it is not the first thing to pass through the cervix then the cervix does not need to dilate enough to pass the head, before other parts of the fetus begin to be delivered.
This leads to compression of the umbilical cord.

369
Q

What are the 3 types of breech?

A
370
Q

What are the different cephalic presentations?

A
371
Q

What is done for an obstetric abdominal examination for determining fetal position?

A

Leopold manoeuvre:
- Superior surface of the fundus is palpated for consistency, shape and mobility.
- Both sides of the uterus are palpated to find which slide the back is facing.
- Which part of the fetus is at the inlet and its mobility.
- Determines fetal attitude and degree of fetal extension into the pelvis.

372
Q

What is felt for in a vaginal examination, when determining fetal position?

A

The sutures of the baby’s head.

373
Q

What are the different frequencies and durations of the contractions during the latent 1st stage, the active 1st stage and second stage of labour?
State what happens to the intensity of the contractions.

A

The intensity of the contractions increase as labour progresses.

374
Q

What are the risk factors for shoulder dystocia?

A
375
Q

What is shoulder dystocia?

A

Vaginal cephalic delivery that requires additional obstetric manoeuvres to deliver the fetus after the head has been delivered.

376
Q

What are the two causes of a shoulder dystocia?

A

The anterior shoulder impacts on the maternal pubic symphysis - more common.
The posterior shoulder impacts on the maternal sacral promontory.

377
Q

What are the complications of shoulder dystocia?

A

Brachial plexus injury.
Neurological dysfunction/ disability - hypoxia.
Neonatal mortality.
Postpartum haemorrhage.
Tare.

378
Q

Where are fetal blood samples taken from during labour, and what are they being checked for?

A

From the head.
They are checking for pH - if the result is of acidosis then it shows hypoxia has occurred.

379
Q

How can labour be induced?

A

Membrane sweep at 39+ weeks.
Prostaglandins - prostin vaginally to soften the cervix.
IV oxytocin.
Artificial membrane ruptures.

380
Q

What does the Bishops score show?

A

How likely it is for induction of labour to be successful.
The higher the scores the greater the chance.

381
Q

What 2 methods can be used for assisted delivery and why may they be required?

A

Forceps and suction cup/ ventouse.

Failure to progress - if the 2nd stage is greater than 2 hours.
Maternal exhaustion.
Maternal conditions - heart disease, etc.
Fetal compromise in the second stage.

382
Q

Why may a caesarean section be required?

A
383
Q

How is glucose metabolism affected by different hormones in pregnancy?

A

Human placental lactogen - increases maternal resistance to insulin.
Progesterone - increases appetite in the first half of pregnancy.
Prolactin - increases maternal insulin resistance.
Oestrogen - increases the release of prolactin.

384
Q

What are the diameters of the pelvic inlet, the mid-cavity and the pelvic outlet?

A

Pelvic inlet - 10.5cm.
Mid-cavity - 12cm.
Pelvic outlet - 11cm.

385
Q

What is restitution in labour?

A

The rotation of the head back to its neutral relation to the shoulders.

386
Q

What are the 4 different types of vulval cancers?

A

Squamous cell carcinoma.
Basal cell carcinoma.
Malignant melanoma.
Soft tissue tumours - fat, blood and nerves.

387
Q

What are the clinical features of vulval cancers?

A

Lumps.
Ulcerations.
Skin changes - pigmentation and sensation.

388
Q

What is seen on histology of squamous cell carcinoma?

A

Keratin pearls.
Atypical squamous cells - large nuclei with a loss of maturation.

389
Q

What is the main metastasis of vulval cancer, and what are the other routes and places that it can metastasise to?

A

Inguinal lymph nodes.

Direct extension - anus, bladder and vagina.
Lymphatic - iliac, para-aortic.
Haematogenous - lungs and liver.

390
Q

What are the viral proteins released by HPV, and what do they do?

A

E6 - inactivates the p53 tumour suppression gene.
E7 - inactive the retinoblastoma tumour suppression gene.

391
Q

What are the different ages and method of the cervical cancer screening programme?

A

25-49 - every 3 years.
50-64 - every 5 years.
Over 65 is only if there has been a recent abnormality.

Using a speculum, cells are scraped from the transformation zone using a brush and tested for HPV.
If positive, the cells are looked at under a microscope.

392
Q

What is the vaccination against HPV, who is it given to and what cancers does it protect against?

A

Gardasil - recombinant vaccine against 6,11,16 and 18 viral subtypes.

It is given to children aged 12-13.

Protects against cervical, vulval, oral and anal cancers.

393
Q

How is invasive cervical cancer staged?

A

FIGO - also used to stage other gynaecological cancers.

394
Q

How is endometrial hyperplasia defined?

A

An increased number of endometrial cells, leading to:
- An increased gland:stroma ratio.
- Thickened endometrium to >7mm.

395
Q

What symptoms can endometrial hyperplasia cause?

A

Inter-menstrual bleeding.
Post-menopausal bleeding.

396
Q

How does serous endometrial adenocarcinoma spread?

A

Exfoliates - breaks off from the primary tumour and travels through the fallopian tubes and deposits of the peritoneal surface.

397
Q

What is the histology of serous endometrial adenocarcinoma?

A

Papillae formed - projections of cells that can break off.
Psammoma bodies.

398
Q

What is the macroscopic appearance of a leiomyoma?

A

Pale, homogenous and well circumscribed mass.

399
Q

What can be done if there is a BRCA1/2 mutation in association with the ovaries?

A

Prophylactic salpingo-oophorectomy.

400
Q

What is a borderline ovarian epithelial tumour?

A

A histological sample that has an atypical appearance and no stromal invasion.

401
Q

What are the 3 subtypes of ovarian teratomas?

A

Mature - benign.
Immature - malignant.
Monodermal - 1 cell type and highly specialised.

402
Q

What do theca and granulosa cell tumours secrete, and what is the effect of this on different patient ages?

A

Oestrogen.

Pre-pubertal:
- Precocious puberty, as the oestrogen accelerates the development of secondary sex characteristics.

Post-pubertal:
- Breast cancer.
- Endometrial hyperplasia and therefore carcinoma.

403
Q

What do leydig and sertoli cell tumours secrete, and what is the effect of this on females of different ages?

A

Testosterone.

Pre-pubertal:
- Prevents normal female pubertal change, preventing female secondary sex characteristics from developing.

Post-pubertal:
- Infertility.
- Amenorrhoea.
- Hirsutism.
- Male pattern baldness.
- Breast atrophy.

404
Q

What cancers can metastasise to the ovary?

A

Breast.
Endometrial, uterine tube or other ovary - other gynae tumours.
Gastrointestinal cancers.
Krukenberg tumours - often gastric with signet cells.

405
Q

In testicular cancers, what are beta-hCG and alpha fetoprotein markers of, respectively?

A

B-hCG - choriocarcinoma (also seen in ovarian).
AFP - yolk sac tumours (also seen in liver).

406
Q

How are dysplastic cervical cells treated?

A

Diathermy - loop biopsy for excision.

407
Q

What is the typical first spread of a cervical carcinoma?

A

Iliac and para-aortic lymph nodes.

408
Q

What can a patient with cervical carcinoma with local spread to the uterus, bladder or rectum present with, generally?

A

Severe pain and fistula formation.

409
Q

What is the patient demographic for endometrial adenocarcinoma?
Why?

A

Peri-menopausal and older women.
They have had an increased lifetime exposure to oestrogen, predisposing them to endometrial hyperplasia and therefore carcinoma.

410
Q

What are symptoms of fibroids?

A

Heavy menstrual loss.
Menorrhagia.
Infertility.
Pressure symptoms on the pelvis due to uterine enlargement - pain, increased urinary frequency, etc.

411
Q

What do malignant ovarian cancer that have spread to the abdomen cause?

A

Ascites, intestinal obstruction and death.

412
Q

What is the pre-invasive precursor of germ cell tumours called?

A

Intratubular germ cell neoplasia.

413
Q

What cells produce the hCG in seminomas of the testes?

A

Seminoma syncytiotrophoblasts.

414
Q

Why is imaging used for the reproductive tract?

A

Aid diagnosis.
Minimises unnecessary intervention and ensures the appropriate intervention is used.
Assessing deeper and distant disease than direct visualisation alone.
Allows for less invasive intervention, for better recovery.
Follow up and surveillance.

415
Q

How are tubo-ovarian abscesses treated?

A

Symptoms control, antibiotics and close observation.

Interventional radiology for drainage or surgery.

416
Q

What is the most common site for pelvic endometriosis, and how is it imaged?

A

Recto-vaginal pouch.

MRI.

417
Q

What is the first line treatment for non-medically manageable fibroids?
Why is it used?

A

Uterine artery embolisation;
- Preserves the uterus and so fertility.
- Can be performed repeatedly.
- Fewer risks than hysterectomy.
- Quicker recovery time.

418
Q

What are some risks of ultrasound?
How is this prevented?

A

Scanning sensitive areas can cause damage to them.
There is a maximum scan time allowed.

419
Q

How is PCOS diagnosed?

A

Based on clinical history and examinations.
Based on ultrasound with:
- Number of follicles pers ovary being 12 or more.

420
Q

Who can ultrasound not be used to diagnose PCOS for, and why?

A

Those within 8 years of menarche or under the age of 20.

There is a high incidence of multi-follicular ovaries at this life stage.

421
Q

What are the two different ring of fires that can be seen on Doppler ultrasound?

A

Corpus luteum cyst - has a fluid-filled centre (left).
Ruptured ectopic pregnancy - has an empty uterus (right).

422
Q

What are ultrasounds used to visualise in the male reproductive tract?

A

Scrotum for germ cell tumours of the testes.
Undescended testes.
Prostate (trans-rectal).
Penis - penile ultrasound.

423
Q

What is peyronie disease?

A

Fibrous tissue plaques within the tunic albugeniea causing painful deformity and shortening of the penis.

424
Q

Who can MRI not be used to scan?

A

Cannot be performed in the first trimester of pregnancy.
Patients with metal work/ implants.

425
Q

What pathologies can MRI be used to scan, in the female and male reproductive tracts?

A

Female:
- Endometrioma.
- Fibroid.
- Ovarian cyst.
- Cervical carcinoma.

Male:
- Prostate cancer.
- Penile fracture.

426
Q

What can fluoroscopy be used to image in the reproductive tracts?

A

Mullerian duct abnormalities.
If the uterine tubes are patent - hyterosalpingogram.

427
Q

What can Müllerian duct anomalies cause?

A

Infertility.
Early pregnancy loss.
Cervical incompetence.

428
Q

Which parts of the male and female reproductive tract are sensitive to ionising radiation?

A

Testes in males.
Ovaries in females.

429
Q

What is Meig’s syndrome?
How is it usually diagnosed?

A

Ascites and pleural effusion, due to a benign, solid ovarian tumour - usually fibroma.

CT scan.

430
Q

What are some oestrogen-mediated changes in the cervix and pelvis that occur to facilitate birth?

A

Cervical softening.
Increased laxity of the pelvic ligaments.

431
Q

What medical treatment can be given for postpartum haemorrhage?
Why?

A

Oxytocin - stimulates contraction of the uterine muscle, contracting the vessels, preventing blood loss.

432
Q

What structures are cut through in a mediolateral episiotomy?

A

Posterior vaginal wall.
Superficial and deep transverse perineal muscles.
Bulbospongiosus of levator ani.
Transverse branches of the pudendal neurovasculature.
Subcutaneous tissue.
Skin.

433
Q

What are the short term risks to FGM?

A

Death.
Haemorrhage.
Infection - HIV, tetanus and gangrene.
Inclusion cysts and keyloid.
Dyspareunia.
Psychological/ psychosexual trauma.

434
Q

What are some obstetric consequences of FGM?

A

Increased likelihood of caesarian section required.
Postpartum haemorrhage.
Episiotomy and tears.
Perinatal death.

435
Q

How long after partum does the midwife have a duty of care to the mother and baby?
Who often takes over care after this?

A

10-28 days.
After this, there is often a healthcare visitor that visits the mother for up to 6 weeks.

436
Q

What is the postpartum period?

A

From delivery of the placenta to 6 weeks afterwards.
It is where the mother reverts back to the pre-pregnancy state.

437
Q

When does the GP perform the postnatal examination and what may it consist of?

A

6 weeks afterwards.

The mothers mental and physical health - blood pressure, urinalysis, general breast, abdominal, and pelvic examinations.
There is also assessment of the feeding and behaviour of the baby.

438
Q

What screening test may be required to wait until after pregnancy?

A

Cervical smear test.

439
Q

What are some lower genital tract changes that occur postpartum?
State why they occur.

A
440
Q

What are some skeletal changes that occur postpartum?

A

Skeletal muscle - stretching of the rectus abdominus muscles resolve, depending on the pre-pregnancy laxity and level of physical activity.
Ligament laxity resolves.

441
Q

What bleeding changes may occur in the postpartum?

A

Initial heavy flow, which decreases until about 6 weeks where it should stop.
Changes in the blood colour from red-brown to red-pink.
Passage of clots for the first 3/4 days.
Period resumption at 6 weeks if no lactation or many months if lactation (up to 6).

442
Q

What are some potential positive psychological changes postpartum?

A

Postnatal high - can still occur after stillbirth.
Increased closeness with the partner and family.
Satisfaction.
Increased closeness with her own mother.
Protectiveness towards the baby.

443
Q

What are some common potential negative psychological changes postpartum?

A

Postnatal blues.
Anxiety and fears of harming the baby.
Overwhelming responsibility.
Resentment or jealousy towards the baby.
Rejection of the baby.

444
Q

How does the mother’s breasts prepare for lactation?

A

Hypertrophy of pre-existing alveolar-lobular structures in the breast.
Formation of new alveolae from budding of the lactiferous ducts.
Proliferation of lactiferous ducts.

445
Q

Why is there minimal milk produced during pregnancy, despite there being high levels of prolactin and placental lactogen?

A

Oestrogen and progesterone inhibit their effect.

446
Q

During lactation, what physiological changes of the breast occur?

A

Increase in size and vasculature of the breast.
Increased budding and branching of the lactiferous ducts.

447
Q

What is milk secretion dependent on?

A

Adequate suckling and production of milk, due to the effects of prolactin.
Adequate emptying of the secreting glands.

448
Q

What occurs to the breast if there is accumulation of milk inside the alveoli?

A

Distension and atrophy of the glandular epithelium.

449
Q

How is oxytocin released?
What inhibits its production?

A

With no inputs, it is released every 90 minutes, in a pulsatile manner.
With sensory inputs - suckling, seeing or hearing, there are increased levels.

Emotional stress or anxiety.

450
Q

What is the let down reflex?

A

Suckling of the breast causes sensory inputs to the hypothalamus and anterior pituitary gland, stimulating an increased synthesis of oxytocin and prolactin, respectively.
Oxytocin travels down into the posterior pituitary to be released, causing contraction of the myoepithelial cells around the alveolae, pushing milk into the milk-collecting ducts.
Prolactin is released from the anterior pituitary, stimulating the lobules within the breast to synthesis more milk.

451
Q

What is the initial breast milk production called?
State its function.

A

Colostrum - high fat content and immunoglobulins.

452
Q

What are the constituents of breast milk?

A
453
Q

What is the protective function of breast milk for the baby?

A

Lactoferrin - binds to iron, preventing proliferation of E.coli.
Aids formation of the gut flora.
Bacteriocidal enzymes
Lymphocytes, polymorphs and plasma cells.
Specific immunoglobulins (A).

454
Q

When should formula feeding be recommended?

A

Severe maternal illness.
Maternal HIV.
Contraindicated maternal medications.

455
Q

What are some breast problems that can be seen postpartum?

A

Nipple sensitivity and pain.
Engorgement - accumulation of milk within the breast which can be very painful.
Mastitis - accumulation of milk within the breast which leads to inflammation and often infection.
Breast abscess - painful buildup of pus within the breast, due to an infection.
Breast lumps - benign or malignant.

456
Q

What is primary postpartum haemorrhage?

A

Loss of 500ml of blood or more from the genital tract within 24 hours of birth of a baby.

457
Q

What are some causes for primary postpartum haemorrhage?
Describe.

A

Atony - relaxation of the uterine muscle, causing dilation of the uterine blood vessels, leading to severe blood loss.
Surgical loss - surgery performed to aid the delivery of the baby.

458
Q

What is secondary postpartum haemorrhage?

A

Abnormal/ excessive bleeding from the genital tract between 24 hours and 12 weeks postnatally.

459
Q

What are some causes of secondary postpartum haemorrhage?

A

Retained products.
Sepsis.

460
Q

How can postpartum haemorrhage be treated mechanically?

A

Bimanual uterine compression.
Catheterisation to empty the bladder.
Surgery.

461
Q

When do postnatal blues peak and what is the treatment?

A

Day 4-5.
Reassurance and support as it is self-limiting in 85% of women.

462
Q

What are the functions of the pelvic floor?

A

Support the pelvic organs - vagina, uterus, ovaries, bladder and rectum.
Maintain urinary and faecal continence.
Facilitate defaecation and mictuition.
Facilitate childbirth.
Sexual function.

463
Q

What is the suspension from the pelvic floor?

A

Vertical support:
- Cardinal ligament = holding the cervix and upper vagina in place.
- Uterosacral ligaments = holding the back of the cervix and upper vagina laterally.
- Round ligament = maintains anteversion of the uterus.

464
Q

What are the attachments of the pelvic floor?

A

Arcus tendinous fascia pelvis - white line.
Endopelvic fascia - stretching from the white line to vaginal wall, medially.

465
Q

What important function does the endopelvic fascia have?

A

Urinary continence - increased intra-abdominal pressure compresses the urethra against it.

466
Q

How is the lower half of the vagina supported?

A

The lower half of the vagina is supported by fusion of the vaginal endopelvic fascia to the:
- Perineal body posteriorly.
- Levator ani laterally.
- Urethra anteriorly.

467
Q

What is the fusion function of the pelvic floor?

A

Linking and connections between the urogenital diaphragm and the perineal body.

468
Q

What forms the pelvic floor?

A

Levator ani muscles.
Urogenital diaphragm.
Perineal body.
Perineal muscles.
Posterior compartment.

469
Q

What composes the levator ani muscle?

A

Puborectalis.
Pubococcygeus.
Iliococcygeus.

470
Q

What are the broad origins and insertions of the levator ani muscle?
State what they overly.

A

Originates from:
- Back of the body of the pubic bone.
- White line.
- Ischial spines.

Inserts:
- Perineal body as they encircle the vagina.
- Lower part of the coccyx.
- Anococcygeal raphe.

They overly the obturator internus muscle.

471
Q

What are the perineal muscles?
State the origins and insertions.

A

Transverse perineal muscles - superifical and deep, originating from the ischium, inserting into the perineal body.

Bulbospongiosus - corpa cavernosa of the clitoris, encircling the vagina, with some originating from the perineal body.

472
Q

What is the urogenital diaphragm?

A

An anterior triangular sheet of dense fibrous tissue.

473
Q

What are the origins and insertions of the urogenital diaphragm?

A

Origin - inferior ischiopubic ramus.
Insertion - urethra, vagina and perineal body.

474
Q

What is the perineal body?

A

A central point between the vagina and rectum.
Point of insertion for the levator ani muscles, and the external anal sphincter.

475
Q

What is the blood supply, lymphatic drainage and nervous supply to the pelvic floor?

A

Blood supply - internal and external pudendal arteries and veins.

Lymphatic - inguinal lymph nodes.

Nervous supply - branches of the pudendal nerve (C2,3,4).

476
Q

What is pelvic organ prolapse, and how common is it?

A

Loss of support for the uterus, bladder, colon or rectum, leading to prolapse into the vagina.

It will be experienced by up to 40% of women.

477
Q

What are the symptoms of pelvic organ prolapse?

A

A dragging sensation or feelings of a lump.
Feelings of incomplete defaecation or mictuition.
Double voiding.
Sexual dysfunction.

478
Q

What are the different types of anterior compartment pelvic organ prolapse?

A

Cystocele - bladder compresses the vagina.
Urethrocoele - urethra compresses the vagina.
Cystourethrocoele - bladder and urethra compresses the vagina.

479
Q

What are middle compartment pelvic organ prolapses?

A

Uterine prolapse - partial prolapse into the vagina, of the uterus.
Procidentia - entire uterine prolapse.
Post-hysterectomy vault prolapse - apex of the vagina may still prolapse.

480
Q

What are posterior compartment pelvic organ prolapses?

A

Rectocele - rectum may prolapse into the posterior part of the vagina.
Enterocele - loops of bowel may prolapse into the pouch of Douglas.

481
Q

What are the causes and risk factors for pelvic organ prolapse?

A

Age.
Parity - particularly vaginal delivery.
Obesity.
Chronic cough (smoking).
Connective tissue disease.
Neurological diseases.
Pregnancy.
Post-menopausal oestrogen deficiency.

482
Q

What is OASIS?

A

Obstetric anal sphincter injuries:
- 3rd and 4th degree tears.
- Leads to issues with continence and support.

483
Q

How is perineal trauma and OASIS prevented?

A

Episiotomy.
Encouraging the mother not to push when crowning.

484
Q

What is the management for pelvic organ prolapse?

A

Surgery - hysterectomy.
Pessaries.

485
Q

What are some posterior compartment pelvic floor dysfunctions?

A

Constipation/ incomplete evacuation.
Anal incontinence due to anal sphincter injury.
Loss of voluntary control of defaecation.