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ESA 4 > Reproductive System > Flashcards

Reproductive System Flashcards

1
Q

What are the female secondary sexual characteristics?

A 
Enlargement of breasts
Growth of body hair
Greater development of muscle behind the femur
Widening of hips, lower waist-hip ratio
Smaller hands and feet
Rounder face
Smaller waist
More subcutaneous fat
Fat deposits in the buttocks, thighs, and hips
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2
Q

What is the urogenital ridge?

A

A region of intermediate mesoderm giving rise to the embryonic kidney and gonad.

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3
Q

Describe the migration of primordial germ cells.

A

Arise in the wall of the yolk sac and migrate to the retro peritoneum, travelling along the dorsal mesentry before arriving at the indifferent gonad. They then populate the mesodermal stroma.

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4
Q

What causes retro peritoneal germ cell tumours to form?

A

They arise if the germ cells fail to migrate properly

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5
Q

What genes on the Y chromosome allow development on the male reproductive system?

A

SRY

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6
Q

Describe the tunica albuginea of the ovaries.

A

A thin layer of connective tissue surrounding the ovary.

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7
Q

Describe the tunica albuginea of the testis.

A

A dense fibrous covering of the testis, which is covered by the tunica vaginalis

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8
Q

Describe the differentiation of the mesonephric duct in males.

A

The ureteric buds and mesonephric ducts make independent openings in the urogenital sinus. The duct then forms the prostate and prostatic urethra.

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9
Q

Describe the differentiation of the mesonephric duct in females.

A

It regresses so the ureteric buds alone enter the urogenital sinus.

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10
Q

What cells produce mullerian inhibiting substance?

A

Leydig cells of the testis

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11
Q

What is the function of mullerian inhibiting substance?

A

Force regression of the paramesonephric ducts in males

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12
Q

Describe differentiation of the paramesonephric ducts in females.

A

Grow and enlarge, drawing together to form the uterus and Fallopian tubes. The paramesonephric ducts and sinus create inductive events, causing the tissue of the sinovaginal bulbs to differentiate and form the vagina, fornix, and hymen. The uterine septum regresses as the cervix forms.

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13
Q

Describe uterus didelphys.

A

2 uterus and 2 vaginas form, resulting from a complete lack of fusion of the paramesonephric ducts.

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14
Q

Describe uterus bicornis.

A

2 separate uteri which join at the cervix and have a common vagina. Caused by a failure of the paramesonephric ducts to fully fuse.

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15
Q

Describe uterus arcuatus.

A

An indentation at the top of the uterus

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16
Q

Describe uterus bicornis unicollis.

A

Complete or partial atresia of one paramesonephric duct, with the rudimentary part lying as an appendage.

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17
Q

Describe cervical atresia.

A

Atresia in both paramesonephric ducts

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18
Q

Describe vaginal atresia

A

The sinovaginal bulbs don’t develop. Small vaginal pouch at the opening of the cervix.

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19
Q

Describe a double vagina.

A

Sinovaginal bulbs fail to fuse.

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20
Q

What are the male secondary sexual characteristics?

A 
Growth of body hair
Greater mass of muscles in front of the femur
Growth of facial hair
Enlargement of the larynx (Adam's apple)
Deeper voice
Increased stature
Heavier skull and bone structure
Increased muscle mass and strength
Larger hands, feet, and nose
Square face
Small waist but wider than females
Increased secretions from oil and sweat glands
Less subcutaneous fat
Higher waist-to-hip ratio
Lower body fat percentage
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21
Q

What are the caudal and cranial attachments of the paramesonephric ducts before differentiation?

A

Caudally - cloaca

Cranially - abdominal cavity

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22
Q

Describe the external undifferentiated genitalia in an embryo.

A

Genital tubercle

Urogenital sinus opening, surrounded by the genital folds, with genital swellings on either side.

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23
Q

Describe the differentiation of the external genitalia in males.

A

The genital tubercle elongates and becomes the glans penis.
The genital folds fuse to form the spongy urethra
The genital swelling becomes the scrotum.

This occurs under the influence of dihydrotestosterone.

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24
Q

Describe hypospadus.

A

Fusion of the urethral folds is incomplete so abnormal openings can form on the ventral surface of the penis.

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25
Q

Describe epispadus.

A

The urethral meatus is found on the dorsum of the penis.

It is often associated with extrophy of the bladder.

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26
Q

Describe the differentiation of the external genitalia in the female.

A

The genital tubercle becomes the clitoris
The genital fold becomes the labia minora
The genital swelling becomes the labia majora

No fusion occurs due to the lack of androgens, and the urethra opens into the vestibule.

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27
Q

Describe the descent of the testes.

A

The gubernaculum pills the testis into the scrotum, through the inguinal canal.
The upper part of the gubernaculum then degenerates, and the lower part persists as the scrotal ligament, which secures the testis to the lower part of the scrotum.

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28
Q

Describe descent of the ovary.

A

The gubernaculum attaches the inferior part of the ovary to the labioscrotal folds. The ovary then descends into the pelvis.
The gubernaculum then develops into the round ligament of the uterus in the inguinal canal.

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29
Q

Describe the effects of congenital adrenal hyperplasia on development of reproductive systems.

A

Decreased steroid hormone production.
In females the effects range from partial masculinisation with a large clitoris to complete male appearance.
In males, masculinisation is inhibited.

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30
Q

Describe androgen insensitivity syndrome in males.

A

Occurs when there is a lack of androgen receptors or a failure of the tissues to respond. The male genitalia don’t differentiate.
As mullerian inhibitory substance is still produced, the mesonephric system is suppressed, so uterine tubes and uterus don’t develop.

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31
Q

Describe 5-alpha reductase deficiency on male development.

A

Causes ambiguous genitalia to form due to an inability to activate testosterone.

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32
Q

Describe Kleinefelter syndrome.

A

XXY
The patient is male with reduced fertility, small testes, and decreased testosterone. They male also have gynaecomastia.
Commonly caused by non-dysjunction of the X chromosomes.

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33
Q

Describe Swyer syndrome.

A

XY with mutations in the SRY genes.

Individuals appear female but won’t menstruate or develop secondary sexual characteristics.

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34
Q

Describe Turner syndrome.

A

45-X
Short stature, high arched palate, webbed neck, shield-shaped chest, cardiac and renal anomalies, inverted nipples, gonadal dysgenesis.

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35
Q

What is gametogenesis?

A

The process of production of mature haploid gametes

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36
Q

Briefly describe the difference between oogenesis and spermatogenesis.

A

Oogenesis - forms an ovum. Very few gametes, intermittent production. 1/400th of the reproductive potential.

Spermatogenesis - forms sperm. Huge number, continuous production. Forms “disposable” cells.

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37
Q

What is the function of meiosis?

A

Reduce the chromosome number to 23
Ensure every gamete is genetically unique
Produce 4 daughter cells

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38
Q

What are the stages of meiosis?

A 
Prophase - chromosomes condense
Metaphase - align in the equator
Anaphase - migrate to opposite poles
Telophase - split
(Twice)
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39
Q

In what stage of meiosis does crossing over occur?

A

Prophase

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40
Q

Where does genetic variation arise from in gamete production?

A

Crossing over
Random segregation
Independent assortment

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41
Q

Describe crossing over in gamete production.

A

Exchange of regions of DNA between two homologous chromosomes (non-sister chromatids). Forms a chiasma.

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42
Q

Where does spermatogenesis occur?

A

Seminiferous tubules

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43
Q

What is the function of tight junctions in the seminiferous tubules?

A

They separate the basal and adluminal compartments, forming the blood-testes barrier.
This maintains the cellular environment for the sperm, and prevents an immune response for the sperm being triggered.

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44
Q

What is the function of the rate testis?

A

Removes fluid to concentrate the sperm.

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45
Q

Where does final maturation of the sperm?

A

Epididymis

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46
Q

What are spermatogonia?

A

The ‘raw material’ for spermatogenesis.

2n

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47
Q

Describe the stages in spermatid formation.

A

Spermatogonium divide to form Ad spermatogonium (maintain stock) and Ap spermatogonium (go into meiosis I).
The ap spermatogonium form secondary spermatocytes, which then go through meiosis II to form spermatids.

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48
Q

What is spermiogenesis?

A

When spermatids cytodifferentiate into spermatozoa.

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49
Q

What is the spermatogenic cycle?

A

The time taken for reappearance of the same stage within a given segment of tubule.
(~16 days in a human)

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50
Q

What is the spermatogenic wave?

A

The distance between the same stage in a tubule.

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51
Q

What is spermiation?

A

When spermatids are released into the lumen of seminiferous tubule.

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52
Q

Describe the path of the sperm as it remodels and matures.

A

Up the seminiferous tubule to the rete testis and through the ducti efferentes into the epididymis.

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53
Q

How are non-motile spermatids transported!

A

Via Sertoli cell secretions, assisted by peristaltic contractions.

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54
Q

How are sperm able to be motile?

A

Through the movement of the flagella

Mitochondria utilise fructose

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55
Q

Describe the contributions from each gland towards semen.

A

Seminal vesicle - amino acid, citrate, fructose, prostaglandins

Prostate - proteolytic enzymes, zinc

Sperm

Bulbourethral - much proteins

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56
Q

What is capacitation?

A

The final maturation step before sperm become fertile, occurring in the female genital tract.

Removal of glycoproteins and cholesterol
Activation of sperm signalling pathways
Allow sperm to bind to the zona pellucida of the oocyte and initiate an acrosome reaction.

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57
Q

Describe the maturation of oocytes before birth.

A

Germ cells which arise from the yolk sac colonise the gonadal cortex and differentiate into oogonia, before proliferating rapidly by mitosis.

By the end of the 3rd months, oogonia are arranged in clusters surrounded by flat epithelial cells of gonadal origin.

The majority of oogonia continue to divide by mitosis, but some enter meiosis. They arrest in prophase I and are called primary oocytes.

Many primary oocytes degenerate by atresia.

All surviving primary oocytes enter meiosis I (committing step) and are individually surrounded by follicular cells.

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58
Q

Describe the pre-antral stage of oocyte maturation during puberty.

A

As primordial follicles begin to grow, the surrounding follicular cells change from flat to cuboidal and proliferate to produce a stratified epithelium of granulosa cells.

The granulosa cells secrete a layer of glycoproteins on the oocyte, forming the zona pellucida which protects the ova.

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59
Q

Describe the antral stage of oocyte maturation during puberty.

A

Fluid filled spaces appear between granulosa cells and coalesce to form the antrum.
Several follicles begin to develop with each ovarian cycle, usually only one reaches maturity.

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60
Q

Describe the ovulation stage of oocyte maturation during puberty.

A

FSH and LH stimulate rapid growth of the follicle several days before ovulation occurs. The mature follicle is now ~2.5cm and is known as a Graafian follicle.
The LH surge increases collagenase activity which facilitates release of the oocyte. Prostaglandins increase the response to LH and cause contraction of the ovarian wall. The oocyte is extruded and breaks free from the ovary.

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61
Q

Describe the appearance of the primary oocyte in the antral stage.

A

Surrounded by the zona pellucida, and cumulus oophorus which is a protective layer and nurtures the oocyte after ovulation.
The antrum is a space above the cell
This is all enclosed by the theca interna, an inner secretory layer which has receptors for LH which causes it to secrete oestrogen
The theca externa forms an outer fibrous layer.

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62
Q

Describe formation of the corpus luteum.

A

Forms as the remaining granulosa and theca interna cells become vascularised. They develop a yellowish pigment and change to lutein cells.
This secretes oestrogen and progesterone, stimulating up the uterine mucosa to enter the secretory phase in preparation for embryo implantation.
It is reabsorbed after 14 days if no fertilisation occurs.

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63
Q

Describe what happens when an oocyte is being ovulated.

A

Fibriae sweep over the surface of the ovary
The Fallopian tube rhythmically contracts.
Fibriae and cilia move the oocyte into the Fallopian tube.
The contractions and cilia move the oocyte into the uterine lumen.

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64
Q

What happens to the corpus luteum if fertilisation doesn’t occur?

A

It degenerates to form fibrotic scar tissue, becoming the corpus albicans.
Progesterone production decreases, precipitating menstrual bleeding

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65
Q

What happens to the corpus luteum if fertilisation does occur?

A

Degeneration of the corpus luteum is prevented by HCG, secreted by the developing embryo. It grows into the corpus luteum of pregnancy (corpus luteum graviditatis)
The cells continue to secrete progesterone until approximately the fourth month, when secretions from the placenta become adequate.

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66
Q

What hormone stimulates follicle growth?

A

FSH

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67
Q

What hormone stimulates follicle maturation?

A

FSH and LH

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68
Q

What hormone promotes development of the corpus luteum?

A

LH

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69
Q

At what hormonal surge does ovulation occur?

A

LH

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70
Q

Where does the pituitary gland sit?

A

Beneath the hypothalamus in the sella turcica (pituitary fossa)

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71
Q

What are the alternative names for the anterior and posterior pituitary?

A

Anterior - adrenohypophysis

Posterior - neurohypophysis

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72
Q

What is the pars tuberalis of the pituitary gland?

A

It wraps the pituitary stalk in a vascularised sheath

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73
Q

What hormones are secreted from the posterior pituitary?

A

ADH and oxytocin

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74
Q

What nuclei in the hypothalamus are ADH and oxytocin secreted from?

A

Paraventricular and supraoptic

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75
Q

What is the upper portion of the neural stalk which extends into the hypothalamus called?

A

Median eminence

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76
Q

What artery connects the anterior pituitary and hypothalamus?

A

Superior hypophyseal artery

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77
Q

What structure does the anterior pituitary arise from?

A

Rathke’s pouch

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78
Q

What are the characteristics of hormones produced by the anterior pituitary?

A

Pulsatile release, synchronised with external signals
Act on specific receptors
Transduce signals via second messengers
Stimulate pituitary hormone release
Stimulate hormone synthesis
Cause hyperplasia and hypertrophy of target cells
Regulate their own receptors

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79
Q

What is the effect of corticotropin releasing hormone on the anterior pituitary?

A

Stimulate ACTH release

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80
Q

What is the effect of thyrotropin releasing hormone on the anterior pituitary?

A

Stimulates TSH and prolactin production

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81
Q

What is the effect of growth hormone releasing hormone on the anterior pituitary?

A

Stimulates growth hormone release

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82
Q

What is the effect of somatostatin on the anterior pituitary?

A

Inhibits growth hormone release

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83
Q

What is the effect of gonadotropin releasing hormone on the anterior pituitary?

A

Stimulate LH and FSH release

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84
Q

What is the effect of prolactin releasing hormone on the anterior pituitary?

A

Stimulate prolactin release

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85
Q

What is the effect of dopamine on the anterior pituitary?

A

Inhibit prolactin release

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86
Q

What cells do FSH and LH act on in females?

A

Ovarian granulosa and theca interna

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87
Q

What cells do LH and FSH act on in males?

A

Sertoli cells and Leydig cells

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88
Q

What effects does testosterone have on gonadotroph secretion?

A

Inhibits GnRH and subsequently causes LH and FSH to fall

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89
Q

What effects does oestrogen have on gonadotroph secretion?

A

Low titres of oestrogen inhibit GnRH secretion

High titres of oestrogen stimulate GnRH secretion, causing an LH surge

Progesterone inhibits the positive feedback effect of oestrogen

Oestrogen affects the amount of GnRH per pulse and progesterone affects the frequency of release

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90
Q

What is the effect of inhibin on gonadotropin secretion?

A

It selectively inhibits FSH secretion

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91
Q

What hormone(s) does Leydig cells secrete?

A

Testosterone

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92
Q

What hormone(s) does Sertoli cells secrete?

A

Androgen binding globulin

Inhibin

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93
Q

What is the effect of testosterone on spermiogenesis?

A

Promotes spermiogenesis

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94
Q

When are testosterone levels highest?

A

In the morning

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95
Q

What is the difference between the uterine and ovarian cycle?

A

The uterine cycle is the preparation of the endometrium

The ovarian cycle is the preparation of the gamete

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96
Q

Describe the changes in the ovary and to gonadotrophs on the at the start of the menstrual cycle (first day of menstruation).

A

Early development of a small group of follicles into the granulosa, which produces low amounts of steroids and inhibin.

Low inhibition of the HPA so FSH and LH increase.

FSH stimulates the mitosis of granuloma cells and follicular development continues.
The theca interna appears, and the follicle is now capable of oestrogen secretion.

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97
Q

Describe the mid follicular phase of the menstrual cycle.

A

A dominant follicle is nominated so further follicles stop developing.
Follicular inhibin increases which selectively inhibits FSH
Follicular oestrogen stimulates the production of gonadotropins in the hypothalamus, subsequently stimulating LH release from the anterior pituitary.

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98
Q

Describe the hormonal changes which prepare the body for ovulation.

A

Circulating oestradiol and inhibin rise, with oestradiol no longer dependent on FSH.
This leads to a surge in LH production, and progesterone production begins in the granulosa cells as they become responsive.
Oestradiol increases sensitivity of the gonadotrophs to increasing LH

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99
Q

Describe what happens to the oocyte at ovulation.

A

Meiosis I ends and meiosis II begins.

The mature oocyte is extruded through the capsule of the ovary.

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100
Q

Describe the changes to the ovary and hormones after ovulation.

A

The follicle is lutenised, secreting oestrogen and progesterone in large quantities and inhibin continues to be produced.

Further gamete development is suspended so the waiting stage is established. Progesterone enhances inhibition by oestrogen so LH is suppressed.

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101
Q

Describe the luteal stage of the menstrual cycle.

A

Progesterone and oestrogens are produced
Increased blood flow causes the luteal layer to become hyperaemic, waiting for the second LH surge. This continues for approximately 14 days.

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102
Q

Describe the difference in hormonal changes depending whether fertilisation occurs or not.

A

No fertilisation causes a dramatic drop in gonadal hormones as the luteum regresses spontaneously, relieving the negative feedback so the HPA can reset.

If fertilisation occurs, the syncytiotrophoblast produces hCG which has a lutenising effect. The corpus luteum then produces steroid hormones to support the pregnancy until the placenta takes over.

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103
Q

What vascular changes occur to cause menses?

A

Ischaemia and necrosis of the spiral arteries

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104
Q

What are the effects of oestrogen throughout the body in the follicular phase of the menstrual cycle?

A 
Increased motility of the fallopian tube
Thickened endometrium
Growth and motility of the myometrium
Thin, alkaline cervical mucosa
Vaginal changes
Changes to the skin, hair, and metabolism
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105
Q

Describe the effects of progesterone throughout the body.

A

Stimulate the secretory form of the endometrium
Increased thickness of the myometrium and reduced motility
Thick, acidic cervical mucosa
Changes to mammary tissue
Increased body temperature and changes to metabolism
Electrolyte changes

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106
Q

How long is the cell cycle?

A

21-35 days

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107
Q

What causes variation in the length of the cell cycle?

A

Due to variation in the length of the follicular phase.

The luteal phase is strictly controlled to 14 days as this is the lifetime of the corpus luteum

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108
Q

What physiological factors can affect the menstrual cycle?

A

Low weight
Emotional stress
Pregnancy
Lactation

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109
Q

What is hydrosalpinx?

A

Infection of the fallopian tube which causes scarring and occlusion at both ends, with fluid accumulating in the centre.

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110
Q

How can appendicitis cause infertility?

A

Inflammation in the abdominal cavity with scarring around the fallopian tubes, blocking them.

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111
Q

How can an ectopic pregnancy cause infertility?

A

If it implants in the fallopian tube, it or surgery to remove it may cause scarring, which would block the tube.

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112
Q

Describe endometriosis.

A

Excessive endometrial growth, which may extend outside the uterus.
Causes heavy, painful, and long menstrual periods, with urinary urgency. There may also be rectal bleeding and premenstrual spotting.
They may be asymptomatic.

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113
Q

Give some causes of oligomenorrhoea.

A

Prolactinoma
Thyrotoxicosis
Grave’s disease
Prader-Willi syndrome

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114
Q

What is the processus vaginalis?

A

An embryonic developmental outpouching of peritoneum which surrounds the testis, epididymis, and the first part of the spermatic cord.

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115
Q

Describe the scrotum.

A

A cutaneous sac which develops from the labioscrotal folds under the influence of dihydrotestosterone.

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116
Q

What is a hydrocoele in the testicles?

A

Serous fluid in the tunica vaginalis due to increased fluid production
Painless
Typically caused by trauma, infection, tumours, or tortion. May be congenital if in children

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117
Q

What is a haematocoele in the testicles?

A

Blood in the tunica vaginalis.

Caused by injury to the scrotum or chronic haemorrhage due to inflammation of the testis.

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118
Q

What is a varicocoele in the testicles?

A

Varicosities in the pampiniform plexus, creating a lumpy swelling in the testicles.
They tend to form during puberty but get larger with age and are mainly unilateral.
They generally form on the left side.

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119
Q

What is a spermatocoele?

A

Epididymal cyst
A painless retention cyst in the epididymis which can be felt as a smooth, firm lump on the top of the testis.
The cause is unknown but may be due to obstruction of the epididymal ducts.

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120
Q

What is epididymitis?

A

Inflammation of the epididymis, commonly caused by STIs.

Can cause a swollen, red, painful testicle.

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121
Q

What is the tunica albuginea?

A

A fibrous capsule surrounding the testis, which seeps into the body of the gonad to form fibrous septae.

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122
Q

What testicular layer does the intestinal coil penetrate through in an indirect inguinal hernia?

A

Tunica vaginalis

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123
Q

Describe the process of the descent of the testes.

A
  1. Gonads develop in the mesonephric ridge near the kidneys
  2. Descend via physical movement and trunk elongation
  3. Cross the inguinal canal obliquely
  4. Push through the deep and superficial inguinal rings
  5. Site themselves in the scrotum
    Pulled by the gubernaculum.
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124
Q

Where does the testicular artery originate?

A

Abdominal aorta

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125
Q

Where does the right testicular vein drain to?

A

Inferior vena cava

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126
Q

Where does the left testicular vein drain into?

A

Left renal vein

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127
Q

What is testicular tortion?

A

Twisting of the testes just above the upper pole.

It is a surgical emergency due to occlusion of the testicular artery, which can lead to necrosis of the testes.

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128
Q

What connects the seminiferous tubules to the epididymis?

A

Efferent ductules and the rete testis

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129
Q

What is the spermatic cord?

A

A passage for structures entering and leaving the testis.

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130
Q

What are the branches of the testicular artery?

A

Cremasteric artery

Artery to vas deferens

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131
Q

What is the name of the network of veins in the testicles?

A

Pampiniform plexus

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132
Q

What is the function of the pampiniform plexus?

A

Wrap around the testicular artery to act as a heat exchanger, cooling the blood entering the testicles

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133
Q

What nerve supplies the testes?

A

Genital branch of the genitofemoral nerve

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134
Q

What lymph nodes does the scrotum drain to?

A

Superficial inguinal nodes

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135
Q

What lymph nodes does the testis drain to?

A

Para-aortic nodes

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136
Q

What are the contents of the spermatic cord?

A 
Testicular artery
Pampiniform plexus
Genital branch of the genitofemoral nerve
Lymphatics
Vas deferens
Processus vaginalis
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137
Q

What is the path of the spermatic cord?

A 
Deep inguinal ring
Lateral to the inferior epigastric vessels
Inguinal canal
Superficial inguinal ring
Posterior border of the testis
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138
Q

Give the layers of the spermatic cord and testis from superficial to deep.

A

External spermatic fascia (aponeurosis of external oblique)
Cremasteric muscle and fascia (internal oblique)
Internal spermatic fascia (transversalis fascia)

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139
Q

Describe the path of the vas deferens

A 
Ascends in the spermatic cord
Through the inguinal canal
Around the pelvic side wall
Joins with the urethra via an ampulla
Opens into the ejaculatory duct
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140
Q

Where are the seminal vesicles found

A

Between the bladder and rectum

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141
Q

What are the seminal vesicles?

A

Diverticulum of the vas deferens, forming a glandular structure

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142
Q

What is the prostate?

A

A fibromuscular gland

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143
Q

Describe the anatomical relationships of the prostate.

A

Base: surrounds the neck of the bladder
Apex: associated with the urethral sphincter and deep perineal muscles
Muscular anterior surface: urethral sphincter
Posterior surface: ampulla of the rectum
Inferolateral: levator ani

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144
Q

What zones tend to be affected by benign prostatic hyperplasia?

A

Central and transitional

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145
Q

What are the symptoms of benign prostatic hyperplasia?

A

Dysuria
Noctiuria
Urgency

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146
Q

What nodes does prostatic malignancy typically spread to?

A

Internal iliac

Sacral

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147
Q

What are the two main dorsal and ventral structures in the penile body?

A

Dorsal - corpora cavernosum

Ventral - corpus spongiosum

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148
Q

What artery supplies the penis?

A

Internal pudendal artery

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149
Q

What is the function of the bulbospongiosus muscle in males?

A

Helps to expel the last drops of urine

Maintain an erection

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150
Q

What is the function of the ischiocavernosus muscle in men?

A

Compresses veins to maintain an erection

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151
Q

What are the parts of the male urethra?

A

Pre prostatic
Prostatic (receives ejaculatory ducts)
Membranous (least distensible as passes through perineum)
Spongy

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152
Q

What is the development of the breast known as?

A

Thelarche

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153
Q

What is development of the axillary and pubic hair known as?

A

Pubarche

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154
Q

What is the first menstrual period known as?

A

Menarche

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155
Q

What is the onset of an increase in adrenal secretions known as?

A

Adrenarche

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156
Q

What is puberty?

A

The stage of human development when sexual maturation and growth are completed, resulting in an ability to reproduce

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157
Q

Give the general sequence of events seen in puberty.

A

Accellerated somatic growth
Maturation of primary sexual characteristic
Appearance of secondary sexual characteristics
Menstruation and spermatogenesis begin

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158
Q

What ends the growth spurt?

A

Epiphyseal fusion

Oestrogen causes this earlier in girls

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159
Q

What is the evidence for body weight having a role in the age of puberty?

A

Obese girls go through early menarche
Malnutrition associated with late menarche
Primary amenorrhoea is common in lean female athletes
Bodyfat set point is very noticeable in girls with fluctuating bodyweight

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160
Q

What cells in males can secrete oestrogen?

A

Sertoli cells

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161
Q

What are the four stages of female puberty?

A

Growth spurt
Breast bud growth
Pubic hair growth
Onset of menstrual cycle

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162
Q

What are the four stages of male puberty?

A

Increased testicular volume
Increased genital size
Growth spurt
Pubic hair growth

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163
Q

What is the start age of female puberty?

A

8-13 years

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164
Q

What is the start age of male puberty?

A

9-14 years

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165
Q

What change in females initiates the first ovarian cycle?

A

The initial LH surge.

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166
Q

What is precocious puberty?

A

When puberty occurs younger than two standard deviations below the average age

Girls below 8
Boys below 9

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167
Q

Give some examples of gonadotrophin dependent (central) precocious puberty

A 
Glioma
Astrocytoma
Hamartoma (pituitary or hypothalamus)
Pineal tumour
hCG secreting germ cell tumours
CNS trauma, infection, surgery, radiation
Hydrocephalus
Arachnoid cyst
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168
Q

What is precocious pseudopuberty?

A

The initiation of early puberty by mechanisms independent of the HPA

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169
Q

Give some examples of gonadotrophin independent (neurological) precocious puberty

A

Congenital adrenal hyperplasia
hCG secreting hepatoma or hepatoblastoma
Choriocarcinoma of the gonads/pineal gland/mediastinum
Ovarian cause masculinisation or feminisation
Leydig cell cause early virilisation
Testotoxicosis
Exogenous oestrogen or androgen exposure, usually iatrogenic

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170
Q

Describe testotoxicosis.

A

An autosomal dominant condition causing male precocious puberty.
Causes rapid physical growth, sexual maturation, and sexually aggressive behaviour in the first 2-3 years.

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171
Q

What is delayed puberty?

A

When the initial features of puberty aren’t present by 13 for girls or 14 for boys
OR
When pubertal development is inappropriate, with more than 5 years between the first signs of puberty and menarche in girls or completion of genital growth in boys.

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172
Q

What are the causes of delayed puberty?

A

Gonadal failure
Turner’s syndrome
Gonadal deficiency
Tumour or radiotherapy affecting hypothalamus or pituitary
Rare gene mutations affecting FSH/LH/receptors

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173
Q

What is Turner’s syndrome?

A

45,X
Causes short stature, gonadal dysgenesis, skeletal abnormalities, cardiac and kidney malformation, dysmorphic face.

There is no mental deficit or impairment of cognitive function.

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174
Q

Describe pre-menopause.

A

Typically occurs from 40 years
Follicular phase of the menstrual cycle shortens. Ovulation is early or absent due to a reduction in oestrogen secretion. FSH and LH rises (FSH more).
Reduced feedback and reduced fertility

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175
Q

Describe menopause.

A

Cessation of menstrual cycles. Occurs at 49-50
No more follicles are left so oestrogen dramatically falls
FSH and LH rise, FSH dramatically as inhibin is lost

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176
Q

What are the physical effects of the menopause throughout the body?

A

Thin cervix
Regression of the endometrium and shrinkage of the myometrium
Vaginal rugae lost
Involution of breast tissue
Changes to skin
Changes to bladder (causes urinary incontinence)
Osteoporosis

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177
Q

What is the adult derivative of the gubernaculum in the female?

A

Round ligament of the ovary

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178
Q

What prevents the primitive ovary descending into the labioscrotal folds?

A

The formation of the uterus by the paramesonephric system, forming a physical barrier

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179
Q

Where does the ovarian artery originate?

A

Abdominal aorta

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180
Q

Where does the right ovarian vein drain into?

A

Inferior vena cava

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181
Q

What does the left ovarian vein drain into?

A

Left renal vein

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182
Q

What is the most superior part of the uterus?

A

Fundus

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183
Q

What part of the uterus is palpable during pregnancy?

A

Fundus

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184
Q

What are the recesses of the vagina which the cervix lies between known as?

A

Fornices

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185
Q

What is the space anterior to the uterus known as?

A

Uterovesicle pouch

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186
Q

What is the space directly behind the uterus known as?

A

Rectouterine pouch

Pouch of Douglas

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187
Q

Describe the course of the round ligament of the uterus.

A

Reflects off the body of the uterus
Through the inguinal canal
Attaches to the labia majora

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188
Q

What lymph nodes drain the labia?

A

Inguinal nodes

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189
Q

What is the normal position of the uterus?

A

Anteverted with respect to the vagina

Anteflexed with respect to the cervix

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190
Q

What are potential symptoms of a retroflexed and retroverted uterus?

A 
Most have no problems. 
Pelvic pain
Irregular or painful menses
Pain with sex
Recurrent urine retention or infections
Miscarriage and problems with IUDs
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191
Q

What ligament provides lateral stability of the cervix, and what is its other function?

A

Transverse cervical ligament

Contributes to the support of the pelvic viscera

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192
Q

What ligament assists with maintaining anteversion of the uterus and opposes the anterior pull of the round ligament?

A

Uterosacral ligament

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193
Q

What is the origin of the uterine artery?

A

Anterior division of the internal iliac artery

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194
Q

What is the origin of the interior pudendal artery?

A

Anterior division of the internal iliac artery

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195
Q

What relationship does the ureter have with the uterine artery?

A

It passes beneath it

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196
Q

What lymph nodes does the ovary drain into?

A

Para aortic
Internal and external iliac
Sacral
Inguinal

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197
Q

What lymph nodes do the body and fundus of the uterus drain into?

A

Para aortic

External iliac

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198
Q

What lymph nodes does the cervix drain to?

A

External and internal iliac
Rectal
Sacral

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199
Q

What lymph nodes does the upper vagina drain to?

A

Internal and external iliac

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200
Q

What lymph nodes does the lower vagina drain to?

A

Inguinal

Sacral

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201
Q

Describe a bimanual examination.

A

Palpate the vaginal walls and cervix for size, shape, and mobility
Palpate the uterus by pressing between the right middle and index fingers, and your left hand on the lower abdomen
Try to palpate the ovaries by placing the internal fingers in the right fornix and trying to press the ovary between them and the other hand. Repeat for the left.

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202
Q

What are the classic signs and symptoms of an ectopic pregnancy?

A

Abdominal pain
Amenorrhoea
Spotting

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203
Q

What are some causes or precipitators for ectopic pregnancy?

A 
Damage or abnormality in the fallopian tubes
  PID
  Tumours
  Sterilisation
IUDs
Previous ectopic pregnancies
Cigarette smoking
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204
Q

What does the labia majora enclose?

A

Pudendal cleft

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205
Q

What does the labia minora enclose?

A

Vestibule of the vagina, including the bulbs and clitoris

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206
Q

Where are Bartholin glands located?

A

Posterior to the vagina

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207
Q

What is a Bartholin’s cyst?

A

When the Bartholin’s duct becomes blocked, causing inflammation of the gland.
Can be caused by an infection, inflammation, or by a physical blockage with mucus. May lead to an abscess.

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208
Q

What are the symptoms of a Bartholin’s cyst?

A

Asymptomatic

Pain when walking, sitting, or during sexual intercourse (dyspareunia)

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209
Q

Where are Skene’s glands located?

A

Anterior wall of the vagina

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210
Q

What is the function of Bartholin’s glands?

A

Secrete mucus to lubricate the vagina

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211
Q

Describe culdocentesis.

A

Drainage of fluid in the pouch of Douglas through the posterior fornix.

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212
Q

What nerve innervates the inferior fifth of the vagina?

A

Pudendal nerve

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213
Q

What innervates the superior 4/5 of the vagina?

A

Uterovaginal plexus

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214
Q

What innervates the uterus?

A

Uterovaginal plexus

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215
Q

What nerves provide sensation of the peritoneum?

A

Pudendal nerve

Ilioinguinal nerve

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216
Q

What ganglia are pain afferents for the internal and external genitalia?

A

Inferior thoracolumbar spinal ganglia

S2-4 spinal ganglia

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217
Q

Describe the course of the pudendal nerve from the pelvis to the perineum.

A

Greater sciatic foramen
Pudendal canal
Lesser sciatic foramen

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218
Q

What are the two significant holes in the pelvic floor?

A

Anterior urogenital hiatus

Central rectal hiatus

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219
Q

What are the functions of the pelvic floor?

A

Support abdominopelvic visca
Resist increased intraabdominal or intrapelvic pressure
Prevent urinary and faecal incontinence

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220
Q

What muscles make up the levator ani, from inner to outer?

A

Puborectalis
Pubococcygeus
Iliococcygeus

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221
Q

What nerve innervates the levator ani?

A

Pudendal nerve

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222
Q

What is the anterior attachment for the levator ani?

A

Pubic bodies of the hip bone

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223
Q

What is the lateral attachment for the levator ani?

A

Tendinous arch

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224
Q

What is the posterior attachment for the levator ani?

A

Ischial spines of the hip bone

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225
Q

What is the main function of puborectalis?

A

Maintain faecal incontinence by creating a 90 degree angle at the anorectal junction

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226
Q

What is the innervation of coccygeus?

A

Anterior rami of S4-5

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227
Q

What are the attachments of coccygeus?

A

Ischial spines to the lateral aspect of the sacrum and coccyx.
Travels along the sacrospinous ligament

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228
Q

What structures are at particularly high risk during childbirth?

A

Pudendal nerve
Levator ani
(Specifically pubococcygeus and puborectalis)

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229
Q

What are the potential consequences of pelvic floor dysfunction?

A 
Stress urinary incontinence
Rectal incontinence
Bladder prolapse
Vaginal prolapse (if damage to the perineal body)
Rectal herniation (if puborectalis torn)
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230
Q

What are the risk factors for pelvic floor dysfunction?

A 
Age
Number of vaginal deliveries
Family history
Weight
Chronic coughing
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231
Q

What is the perineal body?

A

Fibromuscular mass at the junction of the urogenital and anal triangles

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232
Q

What are the functions of the perineal body?

A

Muscle attachment

Tear-resistant body between the vagina and external anal sphincter

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233
Q

What muscles attach to the perineal body?

A 
Levator ani
Bulbospongiosus
Superficial and deep transverse perineal muscles
External anal sphincter
External urethral sphincter
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234
Q

What organisms are particularly implicated in Bartholin’s cysts?

A

Escherichia coli

Staphylococcus aureus

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235
Q

What is the difference between an STI and an STD?

A

STI encompasses both asymptomatic and symptomatic cases of infection where sexual activity is the primary method of transmission.

STD is only symptomatic cases.

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236
Q

Who are the main people at risk of STIs?

A

Young
Ethnic groups
Low socioeconomic status
Aspects of sexual behaviours

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237
Q

What are some reasons for STIs increasing in incidence?

A

Increased transmission with changing sexual and social practices
Increased GUM clinic attendance
Greater public and medical awareness
Improved diagnostic measures

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238
Q

What are the symptoms of human papillomavirus infection?

A

Benign, painless, and verrucous warts

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239
Q

How can you diagnose infection with human papillomavirus?

A

Clinical presentation
Pap smear
Colposcopy with acetowhite test
Cervical swab

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240
Q

What are the consequences of Chlamydia trachomatis infection in men?

A

Urethritis
Epididymitis
Prostatitis
Proctitis

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241
Q

What are the consequences of Chlamydia trachomatis infection in women?

A 
Urethritis
Salpingitis
Cervicitis
Perihepatitis
Pelvic inflammatory disease
242
Q

What are the effects of neonatal chlamydial infection?

A

Conjunctivitis

Pneumonia

243
Q

What is the causative organism of chlamydia?

A

Chlamydia trachomatis

244
Q

How can you diagnose a chlamydia infection?

A

Endocervical or urethral swabs with NAAT if pus present

First void urine with NAAT

245
Q

What are the treatments for chlamydial infection?

A

Azithromycin (single dose)
Doxacycline
Erythromycin (children)

246
Q

What is the benefit of NAAT testing for sexually transmitted infections?

A

It allows dual testing

247
Q

What is the causative organism in syphylis?

A

Treponema pallidum

248
Q

What are the stages of syphylis disease?

A

Primary - painless ulcer (chancre)
Secondary - fever, rash, lymphadenopathy, mucosal lesions
(Latent)
Tertiary - neurosyphylis

249
Q

How can you diagnose a syphylis infection?

A

Serology with an EIA antibody test

Dark field microscopy

250
Q

How can you treat syphylis?

A

Penicillin

251
Q

What are the symptoms of Trichomonas vaginalis infection?

A

Vaginitis with thin, frothy, offensive discharge
Inflammation
Irritation
Dysuria

252
Q

How can you treat Trichomonas vaginalis infection?

A

Metronidazole

253
Q

What is the causative agent in vulvovaginal candidiasis?

A

Candida albicans

254
Q

What are the predisposing factors for vulvovaginal candidiasis?

A 
Antibiotics 
Oral contraceptives
Pregnancy
Obesity
Steroids
Diabetes
255
Q

What are the symptoms of vulvovaginal candidiasis?

A

Profuse, white, itchy, curd-like vaginal discharge

256
Q

How can you diagnose vulvovaginal candidiasis?

A

High vaginal smear

257
Q

How can you treat vulvovaginal candidiasis?

A

Azoles topical
Nystatin topical
Fluconiazole oral

258
Q

What are the symptoms of bacterial vaginosis?

A

Scanty but offensive fishy smelling discharge

259
Q

How can you diagnose bacterial vaginosis?

A

Test vaginal pH
KOH whiff test
Gram stained smear for lactobacilli

260
Q

How can you treat bacterial vaginosis?

A

Metronidazole

261
Q

What is granuloma inguinale?

A

Genital nodules which become ulcers

Caused by Klebsiella granulomatis

262
Q

What are the symptoms of primary genital herpes?

A

Painful genital ulceration
Dysuria
Inguinal lymphadenopathy
Fever

263
Q

Why can genital herpes recur?

A

There is a latent infection in the dorsal root ganglia

264
Q

How can you diagnose genital herpes?

A

PCR of vesicle fluid or a swab of the ulcer base

265
Q

How can you treat primary genital herpes?

A

Aclovir

266
Q

What are the consequences of a gonorrhoea infection in men??

A 
Urethritis
Epididymitis
Procitis
Pharyngitis
Prostatitis
267
Q

What are the consequences of a gonorrhoea infection in women?

A

Urethritis
Endocervicitis
Pelvic inflammatory disease

268
Q

What is the causative agent in gonorrhoea?

A

Neisseria gonorrhoea

269
Q

What are the rare complications of a gonorrhoea infection?

A

Disseminated disease
Arthritis
Skin lesions

270
Q

How can you diagnose a gonorrhoea infection?

A

Swab from the infected site then culture or do NAAT

On the spot diagnosis with a gram stain

271
Q

How can you treat a gonorrhoea infection?

A

Ceftriaxone

Azithromycin (if chlamydia co-infection)

272
Q

What is chancroid?

A

Painful genital ulcers due to Haemophilus ducreyi

273
Q

What is pelvic inflammatory disease?

A

Inflammation close to the womb as a result of infection ascending from the endocervix

274
Q

What are the potential manifestations of pelvic inflammatory disease?

A 
Endometritis
Salpingitis
Parametritis
Oophoritis
Tubo-ovarian abscess
Pelvic peritonitis
275
Q

Why is there an increased risk of ectopic pregnancy in pelvic inflammatory disease?

A

If there is damage to the tubular epithelium, which alters cilial function and may not recover.

276
Q

What is a tubo-ovarian abscess?

A

Inflammation with fibrous exudate into the fallopian tubes. The pus can form adhesions and the accumulation of fluid can lead to swelling of the tubules.
The omentum should contain the infection in the abdomen.

277
Q

What are the risk factors for pelvic inflammatory disease?

A 
Young
No use of barrier contraceptives
Multiple sexual partners
Low socioeconomic background
IUD after insertion or removal
278
Q

What are the symptoms of pelvic inflammatory disease?

A

Lower abdominal pain
Deep pareunia
Abnormal vaginal or cervical discharge and bleeding

279
Q

What are the signs of pelvic inflammatory disease?

A 
Fever
Low, bilateral abdominal tenderness
Cervical motion tenderness
Purulent cervical discharge
Cervicitis
280
Q

What are the differentials with pelvic inflammatory disease?

A 
Ectopic pregnancy
Endometriosis
Ovarian cyst complications e.g. tortion
IBS
Appendicitis
UTI
Functional pain
281
Q

How can you manage pelvic inflammatory disease?

A

Antibiotics - ceftriaxone, doxacycline, metronidazole

Admit for possible surgery if severe

282
Q

What are the potential complications of pelvic inflammatory disease?

A 
Ectopic pregnancy
Infertility
Chronic pelvic pain
Fitz-hugh-curtis syndrome
Reiter syndrome
283
Q

What is Fitz-Hugh-Curtis syndrome?

A

Right upper quadrant pain due to perihepatitis, generally following chlamydial infection

284
Q

What contraception methods can prevent sperm entering the ejaculate?

A

Vasectomy

285
Q

What contraception methods can prevent sperm reaching the cervix?

A

Condoms
Diaphragm
Cervical cap
+/- spermicide

286
Q

What contraceptive methods alter cervical mucus to make it inhospitable for sperm, as well as preventing ovulation?

A

Combined oral contraceptive
Progesterone only pill
Depot progesterone
Progesterone implant

287
Q

How does the combined oral contraceptive pill work?

A

Negative feedback to the HPA inhibits follicular development

Oestrogen loses positive feedback mid-cycle so there is no LH surge

288
Q

How can hormonal contraception impact implantation?

A

Alter the mucus, luteum, and endometrium

289
Q

How can a copper IUD impact implantation?

A

Produces a foreign body reaction and interferes with endometrial enzymes

290
Q

What are the options for emergency contraception?

A

High dose of mixed hormones/progesterone

Mechanical or intrauterine device

291
Q

What is infertility?

A

A failure to conceive within a year of trying.

292
Q

What is the difference between primary and secondary infertility?

A

Primary: Neither partner has ever conceived a child, even if the pregnancy wasn’t successful
Secondary: Either partner has conceived a child, regardless of whether the pregnancy was successful

293
Q

What is vaginismus?

A

Premature contraction of the vaginal musculature, making the vagina too dry and tight to receive the penis.
It can be intolerably painful.

294
Q

What are the symptoms of polycystic ovarian syndrome?

A 
Excessive hair growth
High male hormones
Oligomenorrhoea/amenorrhoea
Acne
Weight gain
295
Q

Give some conditions which can cause anovulation?

A

Polycystic ovarian syndrome
Hyperprolactinaemia
Pituitary dysfunction (micro/macroadenoma, Sheehan’s syndrome)
Turners syndrome
Menopause
Radio/chemotherapy causing ovarian failure

296
Q

What hormone changes would you expect to see in the menopause?

A

Raised LH and FSH

Reduced oestrogen

297
Q

What hormone changes would you expect to see in hypothalamic or pituitary failure?

A

Reduced LH and FSH

Reduced oestrogen

298
Q

What hormone changes would you expect to see in PCOS?

A

Raised LH:FSH ratio

Normal oestrogen

299
Q

What can you use to induce ovulation?

A

Tamoxifen
External synthetic gonadotrophins
GnRH agonist

300
Q

How can you diagnose a tubular occlusion?

A

Hysterosalpingogram

Laparoscopy and dye insufflation

301
Q

What are the potential causes of abnormal sperm production?

A

Testicular disease
Testicular failure
Infection or vasectomy blocking ducts
Hypothalamic or pituitary dysfunction

302
Q

How can you classify normal semen?

A

Volume over 2ml
>20 million sperm per ml
>32% with high motility
>15% normal morphology

303
Q

How long do spermatozoa take to form?

A

74 days

304
Q

Where are spermatozoa produced?

A

Seminiferous tubules (Sertoli cells)

305
Q

Describe the process of spermiogenesis?

A
  1. Nuclear condensation
  2. Acrosome formation (Golgi produce hydrolytic enzymes so the sperm can enter the ovum)
  3. Mitochondria in the midpiece are packed around the contractile filaments
  4. The flagellum is produced by microtubules growing from the centriole to form the axoneme
  5. Cytoplasm and organelles are stripped under the influence of testosterone
306
Q

Where do sperm become motile?

A

Epididymis

307
Q

Where can sperm be stored?

A

Epididymis

308
Q

What happens to sperm if it is not expelled?

A

Phagocytosed by epididymal epithelial cells

309
Q

Describe the excitement stage of coitus in males.

A

The limbic system is stimulated, activating sacral parasympathetic neurons, and inhibiting thoracolumbar sympathetic neurons.
Increased NO production from M3 stimulation causes arteriolar vasodilation in the corpora cavernosa, leading to increased penile blood flow.
The testes elevate and engorge, and the scrotal skin thickens and tenses

310
Q

Describe the plateau stage of coitus in males.

A

The sacrospinous reflex is activated, contracting the ischiocavernosus muscle which compresses the crus penis, impeding venous return and arterial inflow, maintaining the erection.
Stimulation of Cowper’s and Littre’s glands which produce a fluid that neutralises acidic urine and lubricates the distal urethra.
Testes become completely engorged and elevated, the scrotum maintains its state.

311
Q

Describe the emission stage of coitus in males.

A

Stimulation of the thoracolumbar sympathetic neurons, causing contraction of smooth muscle in ductus deferens, ampulla, seminal vesicles, prostate, urethral sphincters, so semen pools in the urethral bulb.

312
Q

Describe the ejaculation stage of coitus in males.

A

The spinal sympathetic reflex is under cortical control, causing contraction of the smooth muscle of glands and ducts, and the internal urethral sphincter
Filling of the internal urethral sphincter stimulates the pudendal nerve, causing contraction of the genital organs, ischiocavernosus, and bulbocavernosus, causing the expulsion of semen.

313
Q

Describe the resolution stage of coitus in males.

A

Activation of the thoracolumbar sympathetic pathway, contracting smooth muscle in the corpora cavernosa to increase venous return.
There is detumescence and flaccidity. The refractory period begins.

314
Q

Describe the excitement stage of coitus in females.

A

Sacral parasympathetic output and inhibition of thoracolumbar sympathetic neurons due to limbic system stimulation.
Vaginal lubrication begins due to vasocongestion and the clitoris engorges with blood. The uterus elevates.
There is increased muscle tone, blood pressure, and heart rate.

315
Q

Describe the plateau stage of coitus in females.

A

Further increase in muscle tone, blood pressure, and heart rate.
Labia minora deepen in colour and the clitoris withdraws under the hood.
Bartholin’s gland secretion lubricates the vestibule for entry of the penis.
The outer third of the vagina forms the orgasmic platform and the inner 2/3 is fully distended

316
Q

Describe the orgasm stage of coitus in women.

A

The orgasmic platform contracts rhythmically 3-15 times.
The uterus and anal sphincter also contract
The clitoris remains retracted
No refractory period so multiple orgasms are possible

317
Q

Describe the resolution stage of coitus for women.

A

The clitoris descends and engorgement subsides
Labia return to normal
Uterus descends
Vagina shortens and narrows

318
Q

What are the changes to the breasts during the sexual response?

A

Excitement - erect nipple, increased size, distended veins
Plateau and orgasm - greater size increase, areola increase in size, sex flush
Resolution - detumescence of areola, return to unaroused state

319
Q

What is the G spot?

A

An area of erotic sensitivity of the anterior wall of the vagina.
The tissue is similar to the male prostate

320
Q

What changes to the sexual response can be seen in older women?

A 
Reduced sexual desire
Reduced vasocongestion
Loss of elasticity in the vagina and urethra
Number of orgasmic contraction reduces
Length and width of vagina decrease
321
Q

What is Klüver-Bucci syndrome?

A

Bilateral medial temporal lobe lesions causing hyperphagia, hypersexuality, hyperorality, visual agnosia, and docility

322
Q

Give some potential causes of male impotence.

A

Tear in the fibrous tissue of the corpora cavernosa
Psychological
Vascular - atherosclerosis/diabetes
Alcohol/antihypertensive

323
Q

How does viagra work?

A

Inhibits cGMP breakdown to increase NO production, increasing blood flow to the penis.

324
Q

What are the components of fluid produced by seminal vesicles?

A

Alkaline fluid
Fructose
Prostaglandins
Clotting factors (semenogelin)

325
Q

What is the function of prostaglandins in seminal fluid?

A

Increased sperm motility and female genital smooth muscle contraction

326
Q

What are the components of the fluid produced by the prostate?

A

Milky and slightly acidic
Proteolytic enzymes
Citric acid
Acid phosphatase

327
Q

What are the components of fluid produced by the bulbourethral (Cowper’s) glands?

A

Alkaline

Mucus

328
Q

What is the cervical mucus like when there is just oestrogen stimulation?

A

Abundant
Clear
Non viscous

329
Q

What is the cervical mucus like when there is oestrogen and progesterone?

A

Thin

Sticky

330
Q

What is the nuclear oocyte maturation?

A

Mitosis I
Nuclear membrane disappears
First polar body separates and enters the perivitelline space
Second meiotic division stalls in metaphase II

331
Q

What is the cytoplasmic oocyte maturation?

A

Organelle distribution - ER and mitochondria to the cortex
Protein and lipid synthesis - cortical granules and lipid droplets
Cytoskeleton dynamics - microfilaments migrate to the cortex

332
Q

How long can sperm live in the female genital tract?

A

5 days

333
Q

How long can oocytes last before phagocytosis if they are not fertilised?

A

6-24

334
Q

Describe the layers of the oocyte before fertilisation.

A

Corona radiata (follicular cells)
Zona pellucida (glycoprotein membrane)
Cytoplasm
Nucleus

335
Q

Where does capacitation of sperm take place and how long does it take?

A

Female genital tract

6-8 hours

336
Q

What happens to capacitate sperm?

A

Protein coat of the cell membrane removed so the enzymes are exposed
Tail movement changes from beating to a whip-like motion

337
Q

What triggers the acrosome reaction in fertilisation?

A

Proteins on the sperm head bind to ZP3 on the zona pellucida

338
Q

What happens in the acrosome reaction?

A

Acrosomal enzymes digest a path through the zona pellucida
One sperm penetrates and the nuclei fuse
Polyspermy blocks are activated.

339
Q

How is the covering of the oocyte directly overlying the chromosomes different to the rest?

A

Smooth and devoid of microvilli

340
Q

What is the fast block to polyspermy?

A

Electrical change from -75mV to +20mV as sodium channels open
Wave of depolarisation begins at the site of entry of the sperm

341
Q

What is the slow block to polyspermy?

A

Calcium released by the ER, inducing local release of cortical granules
Release enzymes to stimulate adjacent release.

342
Q

What is syngamy?

A

When the oocyte completes meiosis II and expels the second polar body, then the pronuclei fuse

343
Q

What is cleavage?

A

Rapid mitotic divisions and metabolic changes so cells divide to form more blastomeres, but the overall size remains the same (G1 and G2 are absent).

344
Q

What is compaction?

A

At the 8 cell stage, blastomeres polarise and form tight junctions to create an inner embryo environment.

345
Q

What is a morula?

A

The 16 blastomere stage, 3-4 days after fertilisation.

346
Q

Approximately how many days after ovulation does implantation occur?

A

6

347
Q

Where are Leydig cells found in the testis?

A

In the perilobular connective tissue surrounding the seminiferous tubules

348
Q

What is the tunica albuginea of the testes?

A

Tough connective tissue covering

349
Q

Where are Sertoli cells found in the testes?

A

Distal part of the seminiferous tubules

350
Q

What is the tunica vasculosa of the testes?

A

Vascular layer divided into lobules by the invaginating tunica albuginea

351
Q

Where are gametes produced in the testis?

A

Seminiferous tubules

352
Q

Describe the path of sperm from the testes out.

A 
Seminiferous tubules
Rete testis
Ductus efferentes
Epididymis
Ductus deferens
Ejaculatory duct
Urethra
353
Q

What are layers of the ejaculatory duct?

A

Pseudostratified columnar epithelium with a few stereocilia
Lamina propria of loose connective tissue
Muscular coat of inner and outer longitudinal layers, and middle circular layers

354
Q

What hormone do sertoli cells secrete?

A

Inhibin

355
Q

What hormone do Leydig cells secrete?

A

Testosterone

356
Q

What is the epithelium of the rete testis?

A

Simple cuboidal

357
Q

What is the characteristic shape of the efferent duct epithelium?

A

Scalloped

358
Q

What is the epithelia of the epididymis?

A

Pseudostratified

359
Q

What are the anatomical borders of the perineum?

A 
Pubic symphysis anterior
Inferior pubic rami and inferior ischial rami anterolateral
Sacrotuberous ligament posterolateral
Coccyx posterior
Pelvic floor roof
Skin and fascia base
360
Q

What are the surface borders of the perineum?

A

Mons pubis/base of the penis - anterior
Medial surface of the thighs - lateral
Superior end of the gluteal cleft - posterior

361
Q

What are the borders of the anal triangle in the perineum?

A

Superior - imaginary line between the ischial tuberosities
Lateral - sacrotuberous ligaments
Posterior - coccyx

362
Q

How many layers of smooth muscle is in the ductus deferens?

A

3

363
Q

What type of epithelium is the ductus deferens?

A

Pseudostratified columnar

364
Q

What type of epithelium is the rete testis?

A

Low cuboidal

365
Q

Is the innervation of the seminal vesicle sympathetic or parasympathetic?

A

Sympathetic

366
Q

What makes up the prostate gland?

A

30-50 tubuloalveolar glands
Inner mucosal glands, middle submucosal, and outer main glands.
Ejaculatory ducts merge with the urethra in the prostate
Fibromuscular stroma

367
Q

What epithelium is in the prostate?

A

Heterogenous (cuboidal, columnar, pseudostratified, simple squamous)

368
Q

What can appear in the prostate gland in older men?

A

Lamellated bodies with proteins, nucleic acid, cholesterol, and calcium phosphate.
May calcify

369
Q

What is the covering of the ovary?

A

Germinated epithelium (peritoneal layer)

370
Q

What is present in the outer cortex of the ovary?

A

Germ cells in various stages of development
Primordial follicle
Single layer of squamous follicular or granulosa cells

371
Q

What is present in the inner medulla of the ovary?

A

Nerves
Blood vessels
Connective tissue
Stromal cells

372
Q

Describe the primordial follicle.

A

Small oocyte surrounded by flat follicular cells

373
Q

Describe the primary follicle.

A

Single layer of cuboidal cells surrounding each oocyte
Granuloma cells give a stratified multilaminar primary follicle
Zona pellucida begins to develop between these layers
Ovarian stromal cells around the oocyte differentiate into theca folliculi which secrete steroid hormones

374
Q

Describe the pre-antral follicle.

A

Theca folliculi is well-established
Well defined zona pellucida
Granulosa at greatest thickness and begins to secrete fluid
Theca folliculi differentiates into the theca interna, which becomes the theca lutein cells that secrete oestrogen
Theca externa forms which is mainly vascular connective tissue

375
Q

Describe the early antral follicle.

A

Coalescing fluid creates spaces between cells of the granuloma layer
Antrum and dominant follicle continue to enlarge.

376
Q

Describe the mature follicle.

A

Corona radiata around the oocyte, formed from a collection of granulosa cells
Growing antrum pushes the oocyte to one side of the follicle where it sits on the cumulus oophorus, which maintains contact with the granulosa, before breaking down just before ovulation so the oocyte and corona radiata can float in the antral fluid
Follicle ruptures as the tissue around it becomes thin and ischaemic

377
Q

Describe the corpus luteum

A

Huge vascularisation

Produces progesterone to prepare the uterine mucosa for implantation.

378
Q

What changes happen to the corpus luteum if implantation doesn’t occur?

A

Fibroses and hyalinised to white connective tissue

379
Q

Why is the epithelium involved in 90% of ovarian cancers?

A

It is constantly being breached and repaired during ovulation

380
Q

Describe the path of the oocyte from the ovary to the uterus

A

Enters the osteum
Widens into the infundibulum
Then becomes the ampulla
Wall thickens and tube narrows to form the isthmus before entry to the uterus

381
Q

Describe the blood supply of the uterus?

A

Paired uterine arteries
Branch to form arcuate arteries in the myometrium
Give rise to straight arteries which supply the stratum basalis and coiled arteries which supply the stratum functionalis

382
Q

What are the layers of the endometrium?

A

Stratum basalis: basal layer with an outer compact and deep spongy layer
Stratum functionalis: Glandular layer which responds to hormonal control. Completely shed in menstruation

383
Q

What are the layers of the uterus?

A

Endometrium with the lamina propria and glands

Myometrium with four layers of smooth muscle

384
Q

Describe the endometrium in the early proliferative phase of the menstrual cycle.

A

Glands are sparse and straight because the endometrial lining has been shed

385
Q

Describe the endometrium in the late proliferative phase of the menstrual cycle.

A

The functionalis is doubled and the glands are now coiled.

This is under the influence of oestrogen, which causes the endometrium to grow.

386
Q

Describe the endometrium in the early secretory phase of the menstrual cycle.

A

Reaches maximum thickness

Pronounced, coiled glands

387
Q

Describe the endometrium in the late secretory phase of the menstrual cycle

A

Glands adopt a ‘sawtooth’ appearance, waiting for maintenance of the endometrium by a conceptus.
If there is no implantation, the spiral arteries spasm, causing ischaemic necrosis.

388
Q

What epithelium is in the endocervical canal?

A

Mucus-secreting simple columnar

389
Q

What epithelium is on the ectocervix?

A

Squamous non-keratinised

390
Q

Where in the cervix do the majority of neoplasms arise?

A

The transformation zone adjacent to the squamocolumnar junction?

391
Q

What epithelium is present in the vagina?

A

Non-keratinised stratified squamous

392
Q

What is the function of glycogen accumulating in the epithelium of the vagina?

A

Substrate for lactobacilli, which metabolise it to regulate vaginal pH

393
Q

What are the layers of the vagina?

A

Epithelium
Mucosa
Submucosa
Muscular (smooth and skeletal)

394
Q

What type of gland is the breast?

A

Compound tubulo-acinar gland

A single lactiferous duct opens from multiple lobes.

395
Q

Describe the difference between inactive and lactating breast tissue.

A

Inactive - limited ductal development, dense interlobular tissue

Lactating - highly developed glands, milk secretions in the alveolar lumen, thin interlobular tissue, vacuolation of secretory cells

396
Q

Where is the location of the nipple in relation to the ribs in young women?

A

5th intercostal space

397
Q

Approximately how many lobules radiate out from each nipple?

A

15-20

398
Q

What connects each lobule to the nipple?

A

Lactiferous sinus

399
Q

What delineates each lobule of the breast?

A

Suspensory ligaments

Fibrous connective tissue

400
Q

What is the rectomammary space?

A

Potential space formed by the breast and fascia overlying the anterior thoracic wall, allowing motility of the breast

401
Q

What lymph nodes does each part of the breast drain into?

A

Lateral - axillary lymph nodes

Medial - parasternal nodes or opposite breast

402
Q

What veins drain the breast?

A

Axillary
Posterior intercostal
Internal thoracic

403
Q

What arteries supply the breast?

A

Internal thoracic
Intercostal
Thoracoacromial

404
Q

What breast changes caused by a tumour could cause dimpling and distortion?

A

Oedema

Shortening of the suspensory ligaments

405
Q

What are the layers of the fallopian tube wall?

A

Inner mucosa (epithelial cells and peg cells)
Muscular
Serosal

406
Q

How does the muscular layer of the fallopian tube change throughout its length?

A

Mostly 2 layers

Thicker in the isthmus with 3 layers

407
Q

What are the function of peg cells in the fallopian tube?

A

Secrete mucus

408
Q

Where is folding in the fallopian tube most pronounced?

A

Ampulla

409
Q

Describe the contents of the anal triangle

A

Anal aperture in the centre, surrounded by the external anal sphincter. Ischioanal fossa laterally which contains fat and connective tissue.

410
Q

What is the function of the ischioanal fossae?

A

Contain fat and connective tissue to aid expansion of the anal canal during defecation.
Extend from the anal region to the pelvic diaphragm.

411
Q

What are the borders of the urogenital triangle?

A

Anterior - pubic symphysis
Lateral - ischiopubic rami
Base imaginary line between ischial tuberosities.

412
Q

From deep to superficial, what are the layers of the urogenital triangle?

A 
Deep perineal pouch
Perineal membrane
Superficial perineal pouch
Deep perineal fascia
Superficial perineal fascia
Skin
413
Q

What is the deep perineal pouch?

A

A potential space between the pelvic floor and perineal membrane.

414
Q

What are the contents of the deep perineal pouch?

A

Part of the urethra
External urethral sphincter
Bulbourethral glands (male)
Deep transverse perineal muscles (male)

415
Q

What is the function of the perineal membrane?

A

To support the pelvic viscera
Attach muscles of superficial external genitalia
Perforated by the urethra and vagina

416
Q

What is the superficial perineal pouch?

A

A potential space between the perineal membrane and fascia

417
Q

What are the contents of the superficial perineal pouch?

A 
Erectile tissue of the penis and clitoris
Ischiocavernosus
Bulbospongiosus
Superficial transverse perineal muscles
Bartholin's glands
418
Q

What is the function of the deep perineal fascia?

A

Cover the superficial perineal muscles

419
Q

What is the superficial perineal fascia continuous with?

A

Superficial fascia of the abdominal wall

420
Q

What are the two layers of the superficial perineal fascia?

A

Superficial and deep

Superficial is fatty, and forms the mons pubis and labia majora

421
Q

As the embryo produces fluid, what happens to the amnion?

A

It is pushed against the chorionic sac to form the amniochorionic membrane, which then produces chorionic villi.

422
Q

What does it mean if the placenta is described as haemochorial?

A

There is a single chorionic layer separating the maternal and foetal circulation

423
Q

What are the aims of placental development?

A

Create a basic unit for exchange to move away from simple diffusion
Anchor the placenta by growth of the outermost cytotrophoblast
Establish maternal blood flow

424
Q

Describe the difference between primary, secondary, and tertiary villi in the placenta.

A

Primary - simple outgrowths of cytotrophoplast and syncytiotrophoblast
Secondary - Mesenchyme grows out into the core during gastrulation
Tertiary - Foetal vessels invade, parenchyme and macrophages also appear

425
Q

What is placenta previa?

A

When the conceptus implants in the lower uterine segment. The placenta may grow across in the internal cervical os, increasing the risk of haemorrhage and blocking the birth canal.

426
Q

What hormone prepares the endometrium for implantation?

A

Progesterone

427
Q

What are pre-decidual cells?

A

The balancing force for invasion of the trophoblast in implantation, preparing the endometrium and stopping implantation going too far.

428
Q

What is placenta accreta?

A

When all or part of the placenta attaches abnormally to the myometrium. The chorionic villa attach to the myometrium rather than being restricted to the decidua basalis.

429
Q

What is placenta increta?

A

Chorionic villi invade into the myometrium

430
Q

What is placenta percreta?

A

Chorionic villi invade through the myometrium

431
Q

How is blood flow improved to the placenta during development?

A

Elaboration of the spiral arteries, creating a low-resistance vascular bed.

432
Q

What causes pre-eclampsia?

A

Inadequate migration of foetal cells so the endothelium remains maternal.

433
Q

What are the effects of pre-eclampsia?

A

The maternal circulation tries to compensate, so blood pressure becomes very high.

434
Q

What is eclampsia?

A

Fitting during pregnancy

435
Q

What is placental insufficiency?

A

Invasion is complete so the developing foetus can’t be fully supported.

436
Q

What are the degrees of monozygotic twins?

A

Separate amnion and chorion
Separate amnion, same chorion
Shared amnion and chorion
(greater sharing changes the risk of problems occurring)

437
Q

What is twin-to-twin transfusion syndrome?

A

A consequence of disproportionate blood supply, resulting in high morbidity and mortality.
Occurs in monochorionic twins
Causes are unknown

438
Q

What is the organisation of the maternal aspect of the placenta?

A

Into cotyledons, which are chorionic villi separated by placental septum.

439
Q

What is the difference between the placenta at the first trimester and the placenta at term?

A

First trimester - thick placental barrier, villi growing in number and size, complete cytotrophoblast layer beneath syncytiotrophoblast layer.

Term - dramatically increased surface area, cytotrophoblast layer lost, thin barrier

440
Q

What hormones are produced by the placenta?

A 
hCG
Progesterone
Oestrogen
hCS
hPL
441
Q

What is the function of hCG produced by the placenta?

A

Supports the corpus luteum until the placenta is large enough.

442
Q

What is the function of progesterone produced by the placenta?

A

Increases appetite to lay down stores

443
Q

What is the function of hCS and hPL produced by the placenta?

A

Increase glucose availability for the foetus, even at the expense of the mother

444
Q

Why is maintenance of oxygen flow to the foetus particularly important?

A

The foetal oxygen stores are very small.

445
Q

What is moved by facilitated diffusion across the placenta?

A

Amino acids
Vitamins
Iron

446
Q

How are immunoglobins transported across the placenta?

A

Mediated by receptors on the surface of the syncytiotrophoblast
Only transports IgG
The exact immunoglobin depends on the pathogens encountered by the mother

447
Q

Give some examples of teratogens.

A 
Thalidomide
Alcohol
Therapeutic drugs
Drugs of abuse
Maternal smoking
448
Q

What is haemolytic disease of the newborn?

A

When the rhesus group of the foetus is incompatible with that of the bother, creating a problem in subsequent pregnancies as the IgG can pass through the placenta.

449
Q

Why does the ABO blood type of the foetus and mother not matter?

A

The ABO antibodies are IgM so can’t pass through the placental barrier

450
Q

Give an example of an infectious agent that can be teratogenic.

A 
Zika
Toxoplasma gondii
Cytomegalovirus
Treponema pallidum
Varicella zoster
Rubella
451
Q

What change in the cardiovascular system occurs during pregnancy?

A

Blood volume increases
Dilation and hypertrophy of the heart
Cardiac output, stroke volume, heart rate increase
Systemic resistance and blood pressure fall

452
Q

Why might there be normal auscultatory changes of the heart during pregnancy?

A

There is dilation and hypertrophy of the heart due to the increased blood volume

453
Q

Why is a normal hypotension seen in trimester 1 and 2?

A

Progesterone relaxes vascular smooth muscle, reducing the total peripheral resistance.

454
Q

Why might there be hypotension in trimester 3?

A

Aortocaval compression by the gravid uterus, reducing blood flow back to the heart.

455
Q

What are the most common reasons for anaemia in pregnant patients?

A

Dilutational anaemia
Iron or folate deficiency
Haemoglobinopathy

456
Q

What would you suspect if a pregnant patient had hypertension?

A

Pre-eclampsia

457
Q

What are the changes in the urinary system during pregnancy?

A

GFR, creatinine clearance, protein clearance, and renal plasma flow increase.
Urea, uric acid, bicarbonate, and creatinine fall
Filtration capacity is intact, but the functional reserve is low.

458
Q

Why would you be unhappy with a urea and creatinine within the usual bounds in a pregnant woman?

A

Creatinine clearance in greater and renal plasma flow is higher in pregnant women, so it should be lower than normal

459
Q

Why are pregnant women at greater risk of hydroureter?

A

Progesterone can relax the smooth muscle of the ureter, or there may be obstruction, which causes urinary stasis

460
Q

What are the complications of UTIs during pregnancy?

A

Pyelonephritis

Pre-term labour

461
Q

What are the changes to the respiratory system during pregnancy?

A

Diaphragm displaced upward, but AP and transverse diameters increase, as well as physiological drive
FRC decreases

462
Q

What causes physiological hyperventilation during pregnancy?

A

Progesterone alters respiratory centres in the brainstem

CO2 production by the foetus increases levels in the body

463
Q

Why are pregnant women at increased risk of metabolic acidosis?

A

They have to compensate for the relative acidosis caused by the high CO2 in the blood, reducing their buffering capacity

464
Q

What stimulates increased maternal peripheral insulin resistance during pregnancy?

A

Human placental lactogen (hPL)

465
Q

What is gestational diabetes?

A

Carbohydrate intolerance confined to pregnancy

466
Q

What are the risks associated with misdiagnosis or poor control of gestational diabetes?

A

Macrosomic foetus
Stillbirth
Congenital defects

467
Q

Why is a pregnant woman at increased risk of ketoacidosis?

A

Lipolysis is increased so there is increased free fatty acid on fasting

468
Q

What are the symptoms of ketoacidosis?

A 
Sweet smelling breath
Abdominal pain
Confusion or agitation
Fatigue
Loss of appetite
Nausea and vomiting
469
Q

What TBG, TSH and free T4 levels would you expect during pregnancy?

A

High TBG and T4

Low TSH

470
Q

What effect does progesterone production in pregnancy have on the GI tract?

A

Relaxes smooth muscle, causing delayed emptying of the bowel and stasis of the biliary tract. (Increases the risk of infection and pancreatitis)

471
Q

Why are pregnant women at increased risk of DVT?

A

Clotting ability
Stasis
Venodilation

472
Q

Why can you not give warfarin to a pregnant women?

A

It freely crosses the placenta

473
Q

Why is pregnancy prothrombic?

A

Fibrinogen and clotting factors increase

474
Q

What adaptions in foetal blood allow it to utilise maternal blood with a low partial pressure of oxygen?

A

Foetal haemoglobin has a higher affinity for oxygen and doesn’t bind 2,3-BPG
High foetal haematocrit

475
Q

Describe the ‘double Bohr effect’ and how it increases oxygen diffusion in the placenta.

A

The CO2 moving into the intervillous blood lowers the pH, and therefore lowers the oxygen affinity of the maternal haemoglobin.
The CO2 lost from the foetal blood increases its pH, increasing the oxygen affinity of the foetal haemoglobin.

476
Q

Describe how the ‘double Haldane effect’ increases CO2 diffusion across the placenta.

A

The maternal haemoglobin must give up its oxygen to accept the carbon dioxide.
The foetal haemoglobin gives up carbon dioxide as oxygen is accepted.

477
Q

What shunts blood past the liver in foetal circulation?

A

Ductus venosus

478
Q

What shunts blood past the lungs in foetal circulation?

A

Ductus arteriosus

479
Q

What shunts blood from the right to the left atrium in foetal circulation?

A

Foramen ovale

480
Q

What separates blood streams in the right atrium to stop oxygenated and deoxygenated blood mixing?

A

Crista dividens

481
Q

Why is it important to shunt blood past the liver in the foetus?

A

The liver is very metabolically active and this is the first entry from the placenta, so it would use up a lot of the oxygen saturated blood.

482
Q

What is the function of the right to left atrial shunt in the foetus?

A

To stop blood circulating the lungs and mixing with unsaturated blood from the body

483
Q

How does the foetus manage transient decreases in oxygenation?

A

Redirects flow to critical organs

Slows the heart rate

484
Q

How is the bradycardia caused when there is low oxygen to the foetus?

A

Low pO2 is detected by chemoreceptors, which stimulates the vagus nerve, subsequently causing a reduction in heart rate

485
Q

What are the potential consequences of chronic hypoxaemia during birth?

A

Growth restriction
Behavioural changes which impact development
Cerebal palsy

486
Q

What are the hormones of foetal growth?

A

Insulin
IGF I
IGF II
Leptin

487
Q

What hormone of foetal growth is nutrient-dependent and at what stage of pregnancy is it used?

A

IGF I

T2/3

488
Q

What hormone of foetal growth is nutrient-independent, what stage of pregnancy is it used, and why is this important?

A

IGF II
T1
It is a time where nutrients may be in low supply due to factors such as morning sickness.

489
Q

What is the dominant cellular growth mechanism in weeks 0-20?

A

Hyperplasia

490
Q

What is the dominant cellular growth mechanism in weeks 20-28?

A

Hyperplasia and hypertrophy

491
Q

What is the dominant cellular growth mechanism in weeks 28 to term?

A

Hypertrophy

492
Q

What is the difference between symmetrical and asymmetrical growth restriction?

A

Symmetrical tends to occur during stages of development with hyperplasia and is irreversible.

Assymetrical tends to occur during stages of development with hypertrophy and is reversible.
It is generally head sparing.

493
Q

Why is jaundice in a newborn common?

A

The foetus cannot conjugate bilirubin, so excretion is handled by the mother. The liver develops its ability to conjugate at birth when the neonate is exposed to light, so this may take time.

494
Q

What periods of development is the crown-rump length important?

A

Pre-embryonic
Embryonic
Early foetal periods

495
Q

What is the main cause of weight gain in the early foetal period?

A

Muscle deposition

496
Q

What is the main cause of weight gain in the late foetal period?

A

Adipose deposition

497
Q

What is the best way to assess foetal growth in the second and third trimesters?

A

Biparietal diameter
Abdominal circumference
Femur length

Using an ultrasound

498
Q

What imaging would you use to assess a pregnancy before 9 weeks?

A

Transvaginal ultrasound

499
Q

What is the main cause of macrosomia?

A

Gestational diabetes

500
Q

What are some reasons for low birth weight?

A

Premature
Constitutionally small
Intrauterine growth restriction (placental insufficiency, twin-twin transfusion syndrome)

501
Q

Describe the development of the respiratory system in weeks 8-16.

A

Pseudoglandular stage

Duct systems form in the bronchopulmonary segments - bronchioles

502
Q

Describe the stages of development of the respiratory system in weeks 16-26.

A

Canalicular stage.

Budding of the respiratory bronchioles from the bronchioles

503
Q

Describe the development of the respiratory system from 26 weeks to term?

A

Terminal sac stage

They bud from the respiratory bronchioles and the type I and II pneumocytes differentiate.

504
Q

What is the function of the ‘breathing’ movements by the foetus?

A

Condition the respiratory musculature ready for birth

Fill the primitive lungs with fluid which is crucial for development.

505
Q

What is neonatal respiratory distress syndrome?

A

Pre-term infants with inadequate surfactant production will have difficulty breathing as the alveoli will be unable to open sufficiently and remain open.

506
Q

How can you reduce the risk of neonatal respiratory distress syndrome when pre-term labour is inevitable?

A

Give corticosteroids to the mother to increase surfactant production in the foetus

507
Q

When is the definitive foetal heart rate established?

A

15 weeks

508
Q

When does foetal kidney function begin?

A

Week 10

509
Q

What needs to develop to allow voluntary, coordinated movement in the foetus?

A

Corticospinal tracts

510
Q

Why are babies relatively uncoordinated and slow?

A

Myelination of the nervous system begins in the ninth month of gestation and continues after birth, so it takes time for them to be able to coordinate movements properly.

511
Q

What is quickening and when does it generally begin?

A 
Maternal awareness of foetal movements. 
17 weeks (variation depending on the mother and whether it is the first pregnancy)
512
Q

When do foetal movements first begin?

A

Week 7

513
Q

What is parturition?

A

The transition from the pregnant state to the non-pregnant state at the end of gestation.

514
Q

What are the three stages of labour (briefly)?

A

Creation of the birth canal
Expulsion of the foetus
Contraction of the uterus and expulsion of the placenta

515
Q

When does the uterus become palpable?

A

12 weeks

516
Q

When does the uterus become palpable at the level of the umbilicus?

A

20 weeks

517
Q

When does the uterus become palpable at the level of the xiphisternum?

A

36 weeks

518
Q

Describe what is meant by the lie of the foetus.

A

Its relationship to the long axis of the uterus

519
Q

What is the normal lie of the foetus at term?

A

Longitudinal

The foetus is usually flexed

520
Q

What is meant by the presentation of the foetus?

A

Which part of the foetus is adjacent to the pelvic inlet?

521
Q

What is the normal presentation of the foetus at term?

A

Cephalic (head first)

522
Q

What is meant by the vertex of the foetus?

A

Relationship of the foetus along its axis and the orientation of the presenting part

523
Q

What is the size of the head in the average foetus at term?

A

9.5cm

524
Q

What is the maximum size of the birth canal in the average woman?

A

11cm

525
Q

What may increase the size of the birth canal?

A

Softening of the ligaments

526
Q

What soft tissues must expand to create the birth canal?

A

Cervix
Vagina
Perineum

527
Q

What are the processes involved in cervical ripening?

A

Reduced collagen and aggregation of the fibres

Increased glycosaminoglycans and hyaluronic acid

528
Q

What are the changes in the myometrium during pregnancy?

A

It is thickened

Produces force when intracellular calcium rises - triggered by action potentials from pacemaker cells

529
Q

What are the uterine contractions which occur during early pregnancy?

A

Low amplitude

Every 30 minutes

530
Q

What are Braxton-Hicks contractions?

A

Small contractions which can be felt but are less frequent than labour as ‘practice’.

531
Q

What are the difference between contractions early and late in labour?

A

Early - variable but high amplitude

Late - more frequent and higher amplitude

532
Q

What hormones make contractions more forceful and how?

A

Prostaglandins release more calcium per action potential

Oxytocin - lowers the threshold to create more action potentials

533
Q

What controls prostaglandin levels?

A

Oestrogen:progesterone levels

high = more

534
Q

Describe the Ferguson reflex?

A

Oxytocin is increased by afferent impulses from the cervix and vagina and act on smooth muscle

535
Q

How does high oestrogen:progesterone ratio promote labour?

A

Increases oxytocin receptors
Increase prostaglandin levels which stimulate uterine contractions
INcreases gap junction communication in smooth muscle cells

536
Q

What is the function of oxytocin in labour?

A

Stimulate the uterus to contract
Stimulate the placenta to make prostaglandins
Increases excitability of the myometrium

537
Q

What is the consequence of prostaglandins released at the onset of labour?

A

The cervix ripens

Contractions become more forceful

538
Q

What is effacement?

A

Thinning and flattening of the cervix

539
Q

What is crowning?

A

When the top of the head appears in the birth canal

540
Q

What is brachystasis?

A

The uterus contracts more than it relaxes as the fibers shorten in the body, driving the presenting part of the foetus to the cervix.

541
Q

What is frank breech?

A

The buttocks in the birth canal with the knees extended

542
Q

What is full breech?

A

The buttocks in the birth canal with the knees flexed.

543
Q

What is a footling breech?

A

When there is a foot in the birth canal

544
Q

Describe the process of the second stage of labour.

A
  1. Head flexes
  2. Head rotates internally
  3. Head stretches the vagina and perineum
  4. Head delivers, rotates, and extends
  5. Shoulders rotate and deliver, rapidly followed by the rest
545
Q

Describe the third stage of labour

A

The effect of uterine contractions is dramatically increased. The uterus contracts down hard, shearing off and expelling the placenta.
Usually occurs within 10 minutes

546
Q

What physiological mechanisms prevent post-partum haemorrhage?

A

Uterine contractions which constricts the blood vessels
Muscle fibres form living ligatures around the maternal blood vessels
Pressure on the placental site by the uterine walls
Blood clotting mechanisms

547
Q

What can be done medically to support the normal mechanisms which prevent post-partum haemorrhage?

A

Oxytocic drug

Manual fundal massage

548
Q

What physical mechanisms promote labour?

A

Mechanical stretching of the uterus increases contractility

Cervical stretching elicits uterine contractions

549
Q

What foetal components promote labour

A

Cortisol from the foetus inhibits progesterone, increasing the action of oestrogen
Foetal oxyytocin

550
Q

What secretes prostaglandins during pregnancy?

A

Placenta
Decidua
Myometrium
Membranes

551
Q

What hormones cause cervical ripening?

A

Oestrogen
Relaxin
Prostaglandins

552
Q

What inhibits the action of oxytocin?

A

Progesterone
Relaxin
Low number of oxytocin receptors

553
Q

What is the latent phase of the first stage of labour?

A

The onset of labour with slow cervical dilation to approximately 4cm, and variable duration

554
Q

What is the active phase of the first stage of labour?

A

Faster rate of cervical change and regular uterine contractions

555
Q

Describe the separation of the placenta from the uterus.

A

The blood in the intervillous space is forced into the veins of the spongy layer of the decidua basilis.
The veins become tense and congested, with pressure maintained by the underlying myometrium.
A living ligature appears around the maternal blood vessels and retract to seal them.
As the placenta pulls away , blood tracks between it and the decidua to complete separation

556
Q

What is normal blood flow through the placental site after birth?

A

500-800ml/min

557
Q

Describe the mammary glands.

A

Lobes containing alveoli, blood vessels, and lactiferous ducts.
There are 15-24 embedded in breast tissue

558
Q

What separates the mammary glands in the breast?

A

Suspensory ligaments of Cooper

559
Q

Describe the development of the breasts in utero.

A

Invagination causes the breast bud to grow
Pits and ducts form in the tissue
Lactiferous ducts are present which are unable to produce milk

560
Q

Describe the development of the breasts in females after puberty?

A

Oestrogen acts on oestrogen receptor alpha to cause tubules to sprout.

Oestrogen acts on oestrogen receptor beta and progesterone on progesterone receptor B to cause squamous to columnar change in the alveoli and hypertrophy.

561
Q

Why do males not usually develop breasts at puberty?

A

Dihydrotestosterone

562
Q

What are the constituents of human milk?

A

90% water
7% sugar (lactose)
3% fat

Proteins, minerals, vitamins

563
Q

What type of sugar is lactose?

A

Disaccharide

Glucose and galactose

564
Q

What is mammogenesis?

A

Substantial development of mammary tissue during pregnancy

565
Q

Describe the changes to the breast during pregnancy

A

Hypertrophy of the system with prominent lobules
Alveolar cells differentiate, capable of lactation by the second trimester

Towards the end of pregnancy the nipple becomes erect and the areola darkens and enlarges. Montgomery tubercles form and the breast becomes more sensitive.

566
Q

What are montgomery tubercles in the breast?

A

Sebaceous glands which fuse with ducts.

Produce oils to protect the breast during feeding and pheromones to direct the baby.

567
Q

What is lactogenesis?

A

The synthesis of milk in alveolar cells from the fat in the SER

568
Q

What is the first thing produced by the mothers breast after giving birth?

A

Colostrum

569
Q

What is colostrum?

A

The first breast secretions which have less water, fat, and sugar than milk produced later.

It is yellow and thick due to increased protein, particularly immunoglobin.

570
Q

How much milk do women produce per day?

A

800ml/day

571
Q

How does oestrogen affect the breast?

A

Stimulates proliferation of the breast and adipose tissue, increases fat metabolismm, and promotes angiogenesis in the surface of the skin (primigravida only).

572
Q

Where is prolactin produced during pregnancy?

A

Decidua

Anterior pituitary

573
Q

What are the effects of prolactin during pregnancy?

A

Lactotroph hypertrophy in the anterior pituitary

Stimulates the production of colostrum

574
Q

What stimulates the production of prolactin after birth?

A

Suckling

575
Q

What is galactokinesis?

A

The let-down reflex stimulated by suckling

576
Q

Describe the let-down reflex

A

Receptors in the nipple stimulate the hypothalamus to produce oxytocin
Oxytocin acts on myoepithelial cells in the breast to eject the milk

577
Q

What is galactopoeisis?

A

The maintenance of milk production

578
Q

Why may the breasts feel lumpy during menstruation?

A

Progesterone and oestrogen cause the growth of alveoli, changing the breast texture.

579
Q

Give some causes of lactation cessation?

A

Not enough suckling, causing turgor of the breast

Suppression of prolactin by ergot preparation, diuretics, retained placenta

Age - mammary gland shrinking begins around 35

580
Q

What is the most likely cause of cyclical and diffuse breast pain?

A

Usually physiological

581
Q

What could be the cause of non-cyclical and focal breast pain?

A

Ruptured cyst
Injury
Inflammation
Breast cancer (only occasionally)

582
Q

What would a milky discharge from the nipple indicate?

A

Endocrine disorder

Medication side effect (OCP)

583
Q

What would a bloody discharge from the nipple indicate?

A

Benign lesion e.g. Duct ectasia, papilloma

Malignant lesion

584
Q

Give some benign causes of a lump in the breast.

A 
Fibroadenoma
Fat necrosis
Lipoma
Leiomyoma
Fibrocystic change
Phyllodes tumour
585
Q

Give some malignant causes of a lump in the breast.

A 
Phyllodes tumour
Hamartoma
Ductal carcinoma in situ
Invasive ductal carcinoma
Invasive lobular carcinoma
Mucinous carcinoma
586
Q

What is a fibroadenoma?

A

A common benign tumour in women below the age of 30.
Tend to be mobile, multiple, and bilateral.

White, fibrous, and rubbery macroscopically.

587
Q

What are phyllodes tumours?

A

Fast growing breast tumours which tend to be benign, but are very aggressive when malignant and often recur.

Histologically: nodes of proliferating stroma covered by epithelium.
Appear leaf-like on the surface

588
Q

Which men are at increased risk of breast malignancy?

A

Klinefelter’s syndrome
MtoF transexual
Men treated with oestrogen for prostate cancer

589
Q

What are the major risk factors for breast cancer?

A

Gender
Uninterrupted menses
Not breastfeeding
Late pregnancy

590
Q

What is the most common presentation of ductal carcinoma in situ?

A

Calcification (linear and branching)

591
Q

What is Paget’s disease of the breast?

A

Inflammation and crusting of the nipple due to ductal carcinoma in situ extending into the nipple skin.

592
Q

How does breast cancer usually metastasise?

A

Through the lymph nides

593
Q

What is peau d’orange?

A

Blockage of the lymphatics in the breast by cancer, causing oedema and pitting.

594
Q

Aside from a lump, what can indicate invasive breast cancer?

A

Paget’s disease of the nipple
Peau d’orange
Inflammation and swelling of the breast
Inverted nipple

595
Q

What is polythelia?

A

A third nipple along the milk line

596
Q

What bacteria is the most common cause of acute mastitis?

A

Staphylococcus aureus

597
Q

Who is most at risk from acute mastitis?

A

Breastfeeding mothers

598
Q

What are the symptoms of acute mastitis?

A

Erythmatous painful breast

Pyrexia

599
Q

What is seen on histological examination of fibrocystic change in the breast?

A

Cyst formation
Fibrosis
Apocrine metaplasia

600
Q

What causes gynaecomastia in men?

A

Transient at the start of puberty as androgen production catches up
Kleinefelter’s syndrome
Oestrogen excess (liver cirrhosis/obesity)
Gonadotrophin excess (functioning testicular tumours, testicular germ cell tumours)
Drug related (spironolactone, cimetidine, alcohol, marijuana)

601
Q

What is the most common type of breast cancer?

A

Invasive ductal carcinoma

ESA 4 (2 decks)

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