Reproductive system Flashcards

1
Q

What is the histology of the seminal vesicles?

A

Slightly coiled tubule, lined by secretory columnar epithelium
Surrounded by 2 layers of smooth muscle and a fibroelastic layer

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2
Q

What is the prostate gland made up of?

A
Made up of 3 concentric rings of glands that are surrounded by smooth muscle and a fibrous capsule. Smooth muscle contracts in ejaculation to squeeze prostatic secretions into the urethra 
Inner periurethral (mucosal) glands - directly surround the urethra so secrete directly into it
Outer periurethral (submucosal) glands - Secrete into urethra via short ducts
Peripheral zone glands - Secrete into urethra via long glands. Is incomplete anteriorly.
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3
Q

When does structural development of the reproductive tract occur?

A

In the embryonic stage of gestation

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4
Q

Where do the gonads derive from?

A

Intermediate mesoderm - part of urogenital ridge

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5
Q

Where do extragonadal germ cells originate?

A

In the yolk sac

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6
Q

What develops if there’s a Y chromosome?

A

Y chromosome contains SRY gene so gonad develops into testis, ducts into male internal genitalia and male external genitalia form?

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7
Q

What develops if conceptus is XX?

A

Gonad develops into ovaries, duct system into tubes and uterus and female external genitalia develop

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8
Q

What do wolffian ducts develop into?

A

In the presence of testosterone, they’re joined by seminiferous tubules and form the epididymis, vas deferens and seminal vesicles

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9
Q

What hormones promote formation of male genitalia rather than female?

A

Testosterone cause persistence of wolffian ducts and is secreted from interstitial cells. Testosterone also causes fusion of genital folds. Sertoli cells secrete mullerian inhibitory hormone to cause regression of mullerian ducts

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10
Q

What reproductive hormones are produced by the hypothalamus?

A

Gonadotrophin releasing hormone
Prolactin releasing hormone
Prolactin inhibiting hormone

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11
Q

What reproductive hormone is released from the posterior pituitary gland?

A

Oxytocin

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12
Q

What reproductive hormones are released from the anterior pituitary gland?

A

FSH, LH, prolactin

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13
Q

What reproductive hormones are released from the gonads?

A

Both produce inhibin.
Testes also produce testosterone and mullerian inhibitory hormone
Ovaries produce oestrogen and progesterone

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14
Q

Which hormones, released by the anterior pituitary gland are glycoprotein hormones?

A

LH, FSH, TSH

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15
Q

Which hormones, released by the anterior pituitary gland are polypeptide hormones?

A

ACTH, MSH, Growth hormone, prolactin

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16
Q

Which hormones exert negative feedback in the HPG axis?

A

Testosterone, Inhibin, moderate oestrogen, progesterone

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17
Q

What hormone exerts positive feedback in the HPG axis?

A

High levels of oestrogen, in the absence of progesterone

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18
Q

What is the action of inhibin and where is it released from?

A

Inhibits FSH release. Released from granulosa cells in the ovary and sertoli cells in the testis.

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19
Q

How do gonadotrophs affect the testes?

A

LH acts on leydig cells to promote testosterone secretion. Testosterone then acts on sertoli cells to promote spermatogenesis . LH is enhanced by inhibin and prolactin. Testosterone also negatively feeds back on LH and GnRH
FSH maintains sertoli cells and makes them responsive to testosterone. Sertoli cells produce inhibin which inhibits FSH and promotes LH

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20
Q

What effects do FSH and LH have on the ovary in the antral phase?

A

LH binds to receptors on theca internal cells which stimulate production of androgens by the theca cells.
FSH binds to granulosa cells which stimulate enzymes production, causing conversion of androgens into oestrogen.

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21
Q

What effects do FSH and LH have on the ovary in the pre-ovulatory phase?

A

Follicle has grown so oestrogen levels are now high.
LH receptors develop on granulosa cells. High oestrogen levels cause positive feedback so there’s a LH surge. This increases production of collagenase so follicle breaks down and ovulation occurs

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22
Q

What effects do FSH and LH have on the ovary in the luteal phase?

A

LH stimulates oestrogen and progesterone production by the corpus luteum. There’s now negative feedback so LH, FSH and GnRH levels fall

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23
Q

What are the regulatory effects of testosterone?

A

Maintains internal genitalia
Anabolic actions
Behavioural effects causing aggression and sexual activity

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24
Q

What effects does oestrogen have on the body?

A
Thin, alkaline cervical mucus
Fallopian tube function
Thickening of endometrium
Growth and motility of myometrium
Skin, hair and metabolism changes
Vaginal changes 
Changes in calcium metabolism
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25
Q

What effects does progesterone have on the body?

A
Thick, acid cervical mucus
Mild anabolic effects
Changes to mammary tissue
Increased thickening of endometrium
Growth and reduced motility of myometrium
Increased body temperature
Electrolyte changes
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26
Q

What are the main stages of the menstrual cycle?

A

Follicular phase which comprises of the menstrual phase and the proliferative phase
Luteal phase or secretory phase

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27
Q

What changes occur to the endometrium in the follicular phase?

A

During the menstrual portion, the necrotic endometrium is shed.
Then, as oestrogen levels begin to rise again after a rest, basal cells of endometrium begin to proliferate and glands are formed but don’t yet secrete.

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28
Q

What happens to the endometrium in the luteal phase?

A

Progesterone released after ovulation causes further proliferation of the endometrium and myometrium but motility of myometrium is reduced. Glands start to secrete a glycogen rich ‘milk’ ready for implantation.
As oestrogen and progesterone decrease, spiral arteries supplying endometrium become ischaemic and so endometrium starts to shed.

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29
Q

How do oestrogen and progesterone differ in the way that they inhibit GnRH?

A

Progesterone reduces the frequency of GnRH pulses while oestrogen reduces the amount that’s released per pulse.

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30
Q

Why might a breast feeding woman not be able to fall pregnant?

A

May have high levels of prolactin. Prolactin disturbs release of GnRH so can affect ovulation and other aspects of fertility.

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31
Q

What are the layers of the capsule that surround the testis?

A

Tunica vasculosa
Tunica albuginea (thick)
Tunica vaginalis

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32
Q

Where are leydig cells found?

A

In islands in between seminiferous tubules of the testes (interstitial cells)

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33
Q

What are the different layers of germ cells in the seminiferous tubules?

A

Deepest are spermatogonia then spermatocytes then spermatids. Scattered throughout are sertoli cells.

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34
Q

What is seen histologically at the junction between the seminiferous tubules and the tubuli recti?

A

A plug of sertoli cells

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35
Q

What epithelium is found in the tubuli recti?

A

Simple cuboidal

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36
Q

What epithelium is found in the rete testis?

A

Simple cuboidal

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37
Q

What epithelium is found in the ductus efferentes?

A

Mixture of simple cuboidal for absorption and simple columnar ciliated for transport

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38
Q

What is the histology of the epididymis tubule?

A

Lined by pseudostratified columnar epithelium with stereocilia on it’s apical membrane. It’s outermost wall contains smooth muscle.

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39
Q

What is the histology of the vas deferens?

A

Folded lumen, lined by pseudostratified columnar epithelium. Also has three muscular layers; a central circular layer and two longitudinal layers either side

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40
Q

What epithelium is found in the seminal vesicles?

A

Pseudostratified columnar that secretes a fluid rich in fructose, prostaglandins and proteins

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41
Q

What are the different layers of glands found in the prostate?

A

All tubuloalveolar glands. From inner- to outermost, they are mucosal, submucosal and main glands

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42
Q

What is the histology of the prostate?

A

Epithelium of glandular element is heterogenous. Surrounded by a fibromuscular capsule that divides the gland into lobules.
Glands sit in a fibromuscular stroma.

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43
Q

What does the prostate gland secrete?

A

Acid phosphatase and prostate specific antigen.

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44
Q

What are prostatic concretions?

A

aka corpora amylacea - lamellated bodies found in the glandular elemnt of the prostate. They contain nucleic acids, proteins, cholesterol and calcium phosphate.

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45
Q

What is contained in the cortex of an immature, prepubertal ovary?

A

Primordial follicles

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46
Q

What affect does FSH have on the pubertal ovary?

A

Stimulates follicle development. Granulosa cells become cuboidal instead of sqaumous and multiple layers form.

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47
Q

What changes occur in the pubertal ovary up until antrium formation?

A

Zona pellucida forms and ovarian stromal cells develop into theca folliculi.
Fluid filled spaces develop between granulosa cells. These grow and coalesce to form an antrum and granulosa cells are pushed to the periphery. Eventually, the oocyte is pushed to one side of the follicle, surrounded by a corona radiata of granulosa cells and sits on a plug of granulosa cells called the cumulus oophorus.
Also in this stage, theca cells differentiate into theca externa and interna

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48
Q

What happens to the follicle in order for ovulation to occur?

A

The cumulus oophorus breaks down and the oocyte and its corona radiate float free in the follicular fluid until tissue surrounding the follicle thins and breaks down, releasing the oocyte into the fallopian tube

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49
Q

What effect does LH have on the follicle after ovulation?

A

Turns granulosa cells into granulosa lutein cells and theca interna cells into theca lutein cells.
Stimulates production of oestrogen and progesterone

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50
Q

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

A

Becomes fibrosed and hyalinised and forms a corpus albicans which normally regresses and is resorbed. Erythrocytes and normally phagocytosed but if this is incomplete then it forms a pigmented remnant - coprus nigricans

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51
Q

What are the histological differences between the ampulla and the isthmus?

A

Ampulla has two smooth muscle layers (longitudinal and circular) and isthmus has 3
Ampulla has mostly ciliated cells and isthmus has higher proportion of peg cells
Mucosa is more folded in ampulla than in isthmus

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52
Q

What epithelia is found in the uterus?

A

Simple columnar

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53
Q

What are the different layers of the uterus?

A

Outer myometrium made up of 4 smooth muscle layers.
Inner endometrium - stratum basalis and stratum functionalis.
Stratum functionalis divides into compact and spongy layers

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54
Q

What is the blood supply to the endometrium?

A

Via uterine arteries which branch to give arcuate arteries.
Arcuate arteries branch to give spiral arteries which supply the functional layer and straight arteries which supply the basal layer

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55
Q

How do the endometrial glands change over the uterine cycle?

A

In proliferative phase, they are straight and start to increase in length. Then, in secretory phase, they grow more than the surrounding lamina propria so they become coiled

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56
Q

What happens to stroma cells in the secretory phase?

A

Develop into decidual cells. These can give rise to placenta and secrete prolactin if implantation occurs

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57
Q

What causes necrosis of endometrium?

A

It’s thought, in absence of fertilisation, prostaglandins are released and these cause spasm of spiral arteries, cutting off nutrients to the functional layer of the endometrium. This causes necrosis of the endometrium

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58
Q

What are the main portions of the cervix?

A

Extends from internal Os to external Os with cervical canal in between

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59
Q

What epithelia is found in the cervix?

A

Cervical canal is lined by simple columnar but this changes to stratified squamous non keratinised roughly at start of external os (this point moves mores inwards throughout life)

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60
Q

How is the vagina lubricated?

A

By mucus secreted by cervical glands and vestibular glands

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61
Q

What is the purpose of glycogen storage by vaginal epithelial cells?

A

It’s metabolism forms acid pH and is used by lactobacilli

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62
Q

What’s the age range for start of puberty in males and females?

A

Males 9-14

Females 8-13

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63
Q

What is the sequence of events of puberty in females?

A
Growth begins
Thelarche
Adrenarche
Growth spurt
Menarche
Adult pubic hair
Adult breasts
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64
Q

What are the different stages of thelarche?

A
1 - pre-pubertal
2 - breast buds form
3 - juvenile smooth contour 
4 - areola and papilla extend above breast
5 - adult contour
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65
Q

What are the different stages of adrenarche?

A

1 - juvenile - no hair
2 - sparse, straight, long, pigmented hair grows mainly along labia/ base of penis
3 - hair is dark, coarser and curlier
4 - hair fulls out towards adult distribution
5 - adult distribution. Extends to medial thigh in males

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66
Q

When does the first ovulation in puberty occur?

A

Roughly 10 months after menarche

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67
Q

What are the main stages seen in male puberty?

A
Genital development
Adrenarche
Spermatogenesis begins
Growth spurt
Adult genitalia
Adult pubic hair
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68
Q

What are the phases of genital development in male puberty?

A

1 - pre-adolescent
2 - Increase in penis length
3 - further increase in length and diameter
4 - development of glans penis and darkening of scrotal skin
5 - adult genitalia

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69
Q

What drives the growth of pubic and axillary hair?

A

Androgens - testosterone in males or androgens from adrenal glands in females

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70
Q

What hormones drive the pubertal growth spurt?

A

Growth hormones and steroids.

In females, oestrogen causes earlier fusion of epiphyses

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71
Q

What are the main known causes of precocious puberty?

A

Neurological due to early stimulation of maturation eg due to meningitis or pineal gland tumous
Uncontrolled secretion of gonadotrophins or steroids ie in a hormone secreting tumour

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72
Q

What’s the pre-menopausal stage?

A

Changes in menstrual cycle due to reduced oestrogen secretion. Decrease in length of follicular phase?

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73
Q

What is the classification of the menopause?

A

6-12 months after last menstruation. No more follicles to be developed and massive decrease in oestrogen and progesterone.

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74
Q

What are the common effects of the menopause?

A
Hot flushes
Collagen loss
Bone breakdown
Painful joints
loss of vaginal rugae and mucus - pain on intercourse
Regression of endometrium and myometrium
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75
Q

What are the advantages of HRT?

A

Relief of menopause symptoms
Increased well being
Can limit osteoporosis

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76
Q

What are the disadvantages of HRT?

A

Increased risk of DVT, cardiovascular disease and breast cancer

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77
Q

What is menorrhagia?

A

Excessively long periods (over 7 days)

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78
Q

What is oligomenorrhoea?

A

Interval between periods > 35 days

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79
Q

What are the main classes of causes of amenorrhoea?

A

Outflow tract
Gonadal
Pituitary/ hypothalamic

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80
Q

What are the main outflow tract causes of amenorrhoea?

A

Primary - imperforate hymen, vaginal atresia, cryptomenorrhoea, mullerian agenesis
Secondary - Intrauterine adhesions ie in asherman’s syndrome

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81
Q

What are the main gonadal causes of amenorrhoea?

A
Primary - Gonadal dysgenesis
Androgen insensitivity syndrome
LH/FSH receptor abnormalities
Congenital adrenal hyperplasia 
Secondary - Pregnancy, anovulation, menopause, premature menopause, polycystic ovarian syndrome, drug induced
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82
Q

What are the main hypothalamic/ pituitary causes of amenorrhoea?

A

Primary - Kallmann syndrome which is disrupted hypothalamus/pituitary interaction
Secondary - sheehan’s syndrome, Exercise amenorrhoea, stress amenorrhoea, eating disorders and weight loss
Hyperprolactinaemia, haemochromatosis
Hypo/hyperthyroidism

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83
Q

How should secondary amenorrhoea be evaluated?

A

Menstrual history, contraception use, any surgery, pregnancy possibility/past, weight change, medication, any chronic disease/stress
Take family history on menopause age, thyroid disfunction, cancer and diabetes
Do physical exam for BMI, hair distribution, thyroid, abdominal masses/tenderness, visual fields

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84
Q

How should amenorrhoea be managed?

A

Take thorough history and make sure possiblity of pregnancy is eliminated.
blood work if indicated by hirsuitism, CNS problems, presence of chronic disease, possible ovarian axis problem

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85
Q

What is dysfunctional uterine bleeding?

A

Excessively heavy, prolonged or frequent bleeding of uterine origin, not due to pregnancy, pelvic of systemic disease

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86
Q

What is the embryological origin of the scrotum?

A

Genital folds

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87
Q

What indicates the bilateral formation of the scrotum?

A

The scrotal raphe, continuous with the penile raphe on the ventral surface of the penis

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88
Q

What is the blood supply of the scrotum?

A

Anterior and posterior scrotal arteries

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89
Q

Where does lymph from the scrotum go to?

A

Superficial inguinal nodes

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90
Q

When is the visceral tunica vaginalis not covering the testis?

A

Where the testis attaches to the epididymis and the spermatic cord

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91
Q

What is the venous drainage of the testes?

A

Right testicular vein drains directly into the abdominal aorta.
Left testicular vein drains into the left renal vein adn then into the abdominal aorta

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92
Q

What are the divisions of the epididymis?

A

Head formed by convergence of ductus efferentes.
Body consisting of single, convoluted tubule
Tail at area of transition between epididymis and vas deferens

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93
Q

What are the contents of the spermatic cord?

A
Vas deferens
Artery to vas deferens
Cremasteric artery 
Testicular artery
Pampiniform plexus of testicular vein
Genital branch of genitofemoral nerve
Lymphatics
Processus vaginalis
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94
Q

What is the passage of spermatic cord and its contents from the abdomen?

A

Exits abdomen through the deep inguinal ring, lateral to the inferior epigastric vessels. Then exits superficial inguinal ring and enters scrotum at posterior of testis.

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95
Q

What are the coverings of the spermatic cord, deep to superficial?

A

Internal spermatic fascia formed by transversalis fasica
Cremasteric fascia and muscle formed by transversalis and internal oblique
External spermatic fascia formed by external oblique aponeurosis

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96
Q

What is the pampiniform plexus?

A

Network of small veins that wrap around the testicular artery, acting as a heat exchanger to cool down the blood that supplies the testes

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97
Q

What are the main important anatomical relationships of the prostate gland?

A
Base - neck of bladder
Apex - urethral sphincter and deep perineal muscles
Muscular anterior - urethral sphincter
Posterior - ampulla of rectum
Inferolateral - levator ani
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98
Q

What are the different segments of erectile tissue in the penis?

A

Pair of corpora cavernosa on dorsum

Single corpus spongiosum on ventral surface

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99
Q

What is the blood supply to the penis?

A

Arterial. Aorta to common iliac to internal iliac to anterior branch of internal iliac to internal pudendal artery
also, cavernous arteries
Venous. Cavernous spaces to venous plexus to deep dorsal vein to prostatic venous plexus to internal iliac vein to common iliac vein to inferior vena cava

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100
Q

What is a hydrocoele?

A

Build up of serous fluid in the tunica vaginalis

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101
Q

What is a haematocoele?

A

Build up of blood in the tunica vaginalis

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102
Q

What is a varicocoele?

A

Varicosity of the pampiniform plexus

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103
Q

On which side of the body are varicocoeles most common?

A

On the left

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104
Q

What is a spermatocoele?

A

Retention cyst in epididymis containing spermatogonia

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105
Q

What’s the difference between oligozoospermia and azoospermia?

A

Oligozoospermia is abnormally low levels of spermatozoa in semen. Azoospermia is the absence of spermatozoa in semen

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106
Q

What is a cryptochid testis?

A

One that is undescended. Sertoli and leydig cells still secrete male sex hormones but germ cells are absent so spermatogenesis is impaired.

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107
Q

What is orchitis and when does it most commonly occur?

A

Inflammation of the testis. Can occur after mumps in puberty

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108
Q

What is testicular torsion?

A

A twisting of the spermatic cord, putting testis at risk of necrosis

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109
Q

By what methods do prostatic malignancies metastasise?

A

Through lymphatics to internal iliac and sacral nodes.

Through venous system and internal vertebral plexus to vertebrae and brain.

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110
Q

What are the features of a gynecoid pelvis?

A
Round pelvic inlet
Straight side walls
Well curved sacral promontory
Not too prominent ischial spines
Sub-pubic arch around 80 degrees
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111
Q

What makes up the pelvic inlet?

A
Sacral promontory
Margins of ala
Arcuate line
Pecten pubis
Pubic crest
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112
Q

What bony landmarks are included in the linea terminalis?

A

Arcuate line, pecten pubis and pubic crest

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113
Q

What makes up the pelvic outlet?

A
Inferior border of body of pubis 
Inferior ramus of pubis
Ramus of ischium
Ishcial tuberosity
Sacrotuberous ligaments
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114
Q

What makes up the true pelvis?

A

The pelvic inlet and outlet

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115
Q

What measurements are taken to asses the pelvic inlet size?

A

Anatomic conjugate from sacral prmontory to superior border of pubic symphysis
Obstetric conjugate from promontory to midpoint of pubic symphysis
Diagonal conjugate from promontory to inferior border of PS

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116
Q

How is the mid-pelvis assessed before childbirth?

A

Check for straight side walls

Measure the bispinous diameter

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117
Q

How is the pelvic outlet assessed?

A

Measure infrapubic angle and the distance between ischial tuberosities

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118
Q

What is a unilaminar primary follicle?

A

When oocyte is surrounded by layer of simple cuboidal cells

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119
Q

What is a multilaminar primary follicle?

A

When the oocyte is surrounded by layer of stratified cuboidal epithelia

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120
Q

What does the theca folliculi secrete?

A

Steroid hormones. Theca cells differentiate from ovarian stromal cells

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121
Q

What does the theca folliculi differentiate into?

A

Theca interna which secretes oestrogen and the theca externa which is vascular connective tissue.

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122
Q

What changes occur in the follicle when fluid filled spaces start to form between granulosa cells?

A

Space pushes granulosa cells to the edge and eventually forms one large antrum. Oocyte is surrounded by few layers of granulosa cells, this is called the corona radiata. Eventually the oocyte is only attached to the edge by a small plug of granulosa cells and this peg is the sumulus oophorus.

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123
Q

What happens to the cumulus oophorus just prior to ovulation?

A

Breaks down so that the oocyte is floating free in the antrum.

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124
Q

What happens to the follicle after ovulation?

A

Granulosa cells convert into granulosa lutein cells and the theca interna cells convert into theca lutein cells. The follicle is now a corpus luteum. This will breakdown after 2 weeks if fertilisation hasn’t occurred.

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125
Q

What is a corpus nigricans?

A

Remnant of the corpus luteum of phagocytosis of its erythrocytes isn’t complete

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126
Q

What types of epithelia line the fallopian tubes?

A

Combination of simple columnar and mucus secreting peg cells. Nearer to the ampulla it’s mostly simple columnar and nearer the isthmus it’s mostly peg cells.

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127
Q

How many smooth muscle layers are found in the fallopian tubes?

A

At the ampulla end, 2 layers and at the isthmus end, 3 layers

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128
Q

What epithelia lines the endometrium?

A

Simple columnar

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129
Q

How can the endometrium be divided?

A

Stratum functionalis which can divide into deep spongy and outer compact
Stratum basalis

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130
Q

What is the blood supply to the endometrium?

A

From paired uterine arteries which branch into arcuate arteries. Arcuate arteries branch into coiled arteries for stratum functionalis and straight arteries in stratum basalis

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131
Q

What hormone drives the proliferative phase of the endometrium?

A

Oestrogen

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132
Q

What happens during the proliferative phase of the endometrium?

A

There’s a regeneration of the stratum funtionalis, from the cells lining the glands in the stratum basalis. There’s an increase in the length of the endometrial glands and a proliferation of the stromal cells that surround the endometrial glands

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133
Q

What drives the secretory phase of the endometrium?

A

Increasing progesterone levels

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134
Q

What happens during the secretory phase of the endometrium?

A

Endometrial glands grow more than the lamina propria and so the glands become coiled. The stroma surrounding the glands become oedematous and stromal cells convert into decidual cells

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135
Q

In the event of fertilisation cells, what’s the purpose of decidual cells?

A

Secrete prolactin and go on to form the placenta

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136
Q

What drives the menstrual phase of the endometrium?

A

Falling progesterone levels in the absence of ferilisation

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137
Q

What happens in the menstrual phase of the endometrium?

A

There’s a spasm of the coiled arteries. There’s therefore lack of blood flow to the stratum functionalis so it becomes necrotic and sheds. This spasm is thought to be due to locally released prostaglandins

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138
Q

Where is the cervix?

A

Connects the uterine cavity with the vagina and it extends from the internal to the external Os. Inbetween these points is the cervical canal.

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139
Q

What epithelium lines the cervix?

A

Mostly simple columnar but just before the external os, it changes to non-keratinised stratified squamous. This point of change gradually moves internally with increasing age

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140
Q

What is the vagina?

A

A fibromuscular tube that connects the cervix to the exterior. Has a muscular layer that contains both skeletal and smooth muscle.

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141
Q

What epithelia lines the vagina?

A

Non-keratinised stratified squamous.

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142
Q

What is the role of glycogen in the vagina?

A

It accumulates in vaginal epithelia under the influence of oestrogen. It is metabolised by lactobacilli and this provides the acid pH of the vagina

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143
Q

What lubricates the vagina?

A

Vagina has no glands so is lubricated by mucus from cervical glands but also by vestibular glands.

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144
Q

What leads to breast enlargement in puberty?

A

Rising oestrogen levels cause accumulation of adipose tissue and lactiferous ducts.

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145
Q

What epithelia lines lactiferous ducts of the breast?

A

First simple cuboidal then simple columnar then stratified squamous at the point of the lactiferous sinuses.

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146
Q

What changes occur in the breast in the menstrual cycle?

A

The oestrogen peak stimulates duct proliferation leading to breast enlargement. There may also be oedema and tenderness.

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147
Q

What changes occur in the breast during pregnancy?

A

Breasts are maximally developed. It’s thought that oestrogen causes duct proliferation and progesterone causes development of secretory tissue. Duct lumens become full of secretory product so secretory cells can appear vacuolated due to fat content of milk

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148
Q

From where do the gonads derive?

A

Intermediate mesoderm as part of the urogenital ridge

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149
Q

What happens to the gonad to convert it from indifferent to sex specific?

A

Shortly after embryonic growth begins, primordial extragonadal germ cells are allocated which arise in the yolk sac and migrate along the dorsal mesentery into the gonads. Then, depending on the sex chromosomes present, reproductive system development continues

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150
Q

How does the SRY gene drive male development?

A

It’s located on the Y sex chromosome and drives the development of the gonads into the testes and the development of the external and internal genitalia

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151
Q

What does the gonad develop into with XX sex chromosomes?

A

Ovary

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152
Q

What does the male duct system comprise of?

A

Epididymis, vas deferens and urethra

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153
Q

What does the female external genitalia consist of?

A

Vagina, vestibule, labia minor and majora, and the clitoris

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154
Q

What are some male secondary sexual characteristics?

A
Relatively large body size
Smell
Body hair distribution
Male pattern baldness
Coarser hair and skin
Body shape
Fat distribution
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155
Q

What are some female secondary sexual characteristics?

A
Relatively small body size
Subcutaneous fat distribution
Smoother hair and skin
Breast development
Central nervous effects
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156
Q

How does testosterone affect the mesonephric and paramesonephric ducts?

A

Helps maintain them

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157
Q

What’s another word for the mesonephric ducts?

A

Wolffian ducts

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158
Q

What’s another name for the paramesonephric ducts?

A

Mullerian ducts

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159
Q

What do the mesonephric ducts go on to form, in the presence of testosterone?

A

They’re joined by the seminiferous tubules at the rete testis. The remainder forms the vas deferens, epididymis and seminal vesicles

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160
Q

Where is mullerian inhibitory hormone secreted?

A

By sertoli cells lining the seminiferous tubules

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161
Q

What effects does mullerian inhibitory hormone have?

A

Causes regression of the paramesonephric ducts

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162
Q

What happens to the paramesonephric ducts in the absence of mullerian inhibitory hormone?

A

Start as invaginations of the urogenital ridge epithelium. Then, with embryonic folding, fuse to form the uterus, fallopian tubes, vagina and cervix.

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163
Q

How are the vagina and cervix formed?

A

Sinovaginal bulb forms above the urogenital sinus this grows to form the vagina. Vagina is separated partly from the outside by the hymen

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164
Q

How do the testes descend?

A

Start off in the upper lumbar area and as the body grows, they’re brought more caudally. They’re tethered to the labioscrotal folds by the gubernaculum.
A musculofascial layer evaginates into the scrotum, bringing the peritoneum to form the processus vaginalis.
Testes then migrate over the pubic bone until they reach the scrotum and are surrounded by the processus vaginalis. They pass through the inguinal canal.

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165
Q

How is the spermatic cord formed?

A

From fascial layers, the obliterated stem of processus vaginalis, vas deferens and the testicular vessels and nerves

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166
Q

What is the remnant of the gubernaculum?

A

Scrotal ligament in males

Round ligament of uterus in females

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167
Q

What are the different types of hypospadias?

A

First degree - orifice opens onto glans penis
Second degree - urethral orifice opens on to shaft
Third degree - orifice opens onto perineum

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168
Q

What is a bicornuate uterus and what are some consequences?

A

When fusion of mullerian ducts is improper or incomplete so that the cephalic portion of the uterus is bifurcated. Causes problematic pregnancies with recurrent pregnancy loss, pre term births, breech births and deformity.

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169
Q

What’s the advantage of the testes being suspended outside of the body by the spermatic cord?

A

Keeps them slightly cooler than the rest of the body. This means that if the body temperature rises the sperm production won’t be affected

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170
Q

What are the components of the capsule surrounding the testis?

A
From innrer to outermost
Thick tunica albuginea which also extends into fibrous septa which divide the testes into lobules containing seminiferous tubules. 
Tunica vasculosa
Tunica vaginalis
Scrotum
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171
Q

What are the two types of cells that line the seminiferous tubules?

A

Sertoli cells which secrete mullerian inhibitory hormone but also support developing sperm and secrete testicular fluid into the tubules
Spermatogonia which undergo meiosis to give rise to spermatozoa

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172
Q

What is spermatogenesis?

A

The process through which diploid spermatogonia stem cells undergo meiosis to become haploid spermatozoa.

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173
Q

What divisions do spermatogonia undergo in spermatogenesis?

A

Mitosis - primary spermatocytes
Meiosis - Secondary spermatocytes
Meiosis - Spermatids

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174
Q

When are cytoplasmic bridges of spermatocytes broken?

A

When the leave the seminiferous tubules

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175
Q

Where does spermatogenesis take place?

A

Divisions take place between sertoli cells. After this, Spermatids are remodelled within the sertoli cells and then pass into the rete testis, ductus efferentes and epididymis, maturing the whole time until they become spermatozoa

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176
Q

What’s a spermatogenic cycle?

A

New cycles of spermatogenesis that start every 16 days

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177
Q

What’s a spermatogenic wave?

A

New spermatogenic cycles starting at new points all along the seminiferous tubules so that sperm is constantly being produced

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178
Q

What are the 3 parts of the epididymis?

A

Head - Superior section and point of entry for ductus efferentes
Body - middles section
Tail - Inferior section, continuous with the vas deferens

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179
Q

What separates the epididymis from the testis?

A

Tunica vasculosa and tunica albuginea

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180
Q

What is the purpose of the vas deferens?

A

Transports sperm from the epididymis to the ejaculatory duct during the emission phase of ejaculation. Has 3 smooth muscle layers to aid with ejaculation

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181
Q

What do the seminal vesicles secrete?

A

Fructose rich, alkaline fluid forming 70% of ejaculated semen

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182
Q

What does the prostate gland secrete?

A

Seminal fluid rich in bicarbonate buffers, citric acid and fibrinolytic enzyme

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183
Q

What’s the importance of the bicarbonate buffers in prostate secretions?

A

Helps to neutralise the acidity of the vagina.

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184
Q

What’s the purpose of the fibrinolytic enzyme in prostate secretions?

A

Liquefies semen

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185
Q

What does the secretory activity of the prostate depend on?

A

Testosterone levels

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186
Q

What’s the purpose of the bulbourethral glands?

A

Secrete sugar rich mucus into the membranous urethra to lubricate the urethra. It also contributes to pre-ejaculatory emissions

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187
Q

Where is the infundibulum in relation to the ovary?

A

Lies lateral to it

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188
Q

What are the three components of the ovary?

A

Surface - covered in germinal simple cuboidal epithelium that’s continuous with the peritoneum.
Cortex - Made up of stroma tissue that supports follicles. Made up of spindle cells, ground substance and collagen cells. Has superficial cortex, or tunica albuginea that’s more fibrous than the deep cortex
Medulla - Made of supporting stroma with a rich network of vessels and nerves

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189
Q

What peritoneal ligaments does the ovary attach to?

A

Suspensory ligament that attaches mesovarium to the pelvic wall
Round ligament that connects the ovary to the fundus of the uterus

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190
Q

What is oogenesis?

A

The process by which oogonia undergo meiosis to form primary oocytes

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191
Q

How do granulosa cells influence oogenesis?

A

Stimulate oogonia entry into oogenesis and then pause process at meiosis by secreting Oocyte Maturation Inhibitor. Oocytes are kept at this stage until puberty

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192
Q

What are the 3 main phases of follicle development before ovulation?

A

Pre antral follicle - Zona pellucida forms between oocyte and granulosa cells. Receptors develop on granulosa cells for oestrogen and FSH and on thecal cells for LH
Antral follicle - fluid filled antrum forms. Thecal cells bind LH and are then stimulated to synthesise androgens which are then converted to oestrogen by the granulosa cells. Oestrogen and FSH stimulate the development of LH receptors on granulosa cells.
Pre-ovulatory follicle - Primary oocyte’s stimulated by LH surge to undergo meiosis and form and secondary oocyte and the first polar body. Granulosa cells start to produce progesterone and then the follicle ruptures and ovulation occurs

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193
Q

What hormones does the corpus luteum secrete?

A

Oestrogen and progesterone

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194
Q

What reproductive hormones are released by the hypothalamus?

A

Gonadotrophin releasing hormone (GnRH)
Prolactin releasing hormone
Prolactin inhibiting hormone

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195
Q

What reproductive hormones are released by the posterior pituitary gland?

A

Oxytocin

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196
Q

What reproductive hormones are released by the testes?

A

Testosterone
Inhibin
Mullerian inhibiting hormone

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197
Q

What reproductive hormones are released by the anterior pituitary gland?

A

Follicle stimulating hormone
Luteinising hormone
Prolactin

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198
Q

What reproductive hormones are released by the ovaries?

A

Oestrogen
Progesterone
Inhibin

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199
Q

What reproductive hormones are released by the placenta?

A

Human chorionic gonadotrophin
Human placental lactogen
Progesterone
Oestrogen

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200
Q

What cell type secretes prolactin in the anterior pituitary gland and what does prolactin do?

A

Lactotrophs. Stimulates oestrogen and progesterone and milk production

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201
Q

What affects release of GnRH from the hypothalamus?

A
Environmental factors
Weight
Oestrogen
Progesterone
Testosterone
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202
Q

In what kind of pattern is the release of GnRH?

A

Pulsatile, roughly once an hour

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203
Q

What hormones exert negative feedback on GnRH secretion by the hypothalamus?

A

Testosterone
Moderate oestrogen (reduces amount released)
Progesterone (reduces frequency)

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204
Q

What hormones exert positive feedback on GnRH secretion by the hypothalamus?

A

High oestrogen, in the absence of progesterone

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205
Q

What hormones exert negative feedback on LH release by the anterior pituitary?

A

Testosterone
Moderate oestrogen
Progesterone

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206
Q

What hormones exert negative feedback on FSH release by the anterior pituitary?

A

Testosterone
Moderate oestrogen
Progesterone
Inhibin

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207
Q

What cells secrete inhibin?

A

Sertoli cells in seminiferous tubules

Granulosa cells

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208
Q

What hormones exert positive feedback on LH production in the male?

A

Inhibin

Prolactin

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209
Q

What action does LH have in the male?

A

Acts on leydig cells to stimulate them to produce testosterone

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210
Q

What action does FSH have in the male?

A

Acts on Sertoli cells which support spermatogenesis and also release inhibin

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211
Q

At which follicular stages is negative feedback exerted on GnRH release from the hypothalamus?

A

Antral. Oestrogen levels are moderate as follicle is in primitive stages so is small. The larger the follicle, the more oestrogen is produced.
Luteal - corpus luteum produces oestrogen and progesterone, as stimulated by LH. Progesterone blocks the positive feedback of the high oestrogen levels.

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212
Q

At what follicular stage is positive feedback exerted on the hypothalamus?

A

Pre ovulatory. Follicle is growing so oestrogen levels are rising. There is no progesterone so oestrogen exerts positive feedback. LH and FSH rise although FSH less due to negative feedback from inhibin.

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213
Q

What is meant by a determinative effect?

A

Means it is only partly, or not at all reversible

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214
Q

What is meant by a regulatory effect?

A

One that is highly reversible and requires constant (hormonal) stimulation for maintenance

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215
Q

What are some determinative effects of testosterone?

A
Facial and body hair
Increased size and mass of muscle, bone and vocal cords.
Increased stature
Deepening of voice
Growth of penis
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216
Q

What are some regulatory effects of testosterone?

A

Maintenance of internal genitalia
Anabolic actions
Behavioural effects

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217
Q

What are the main effects of oestrogen?

A
Thin, alkaline cervical mucus
Fallopian tube function
Endometrial thickening
Myometrial thickening and motility
Skin, hair and metabolic changes
Vaginal changes
Increased calcium resorption
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218
Q

What are the main effects of progesterone?

A

Thick, acid cervical mucus
Catabolic changes
Endometrial thickening into secretory form
Myometrial thickening but reduced motility
Mammary tissue changes
Increased body temperature
Electrolyte changes

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219
Q

In the menstrual cycle, what can the follicular phase be further subdivided into?

A

Menstrual phase days 0-4

Proliferative phase days 5-14

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220
Q

What’s the main purpose of the follicular phase of the menstrual cycle?

A

Follicle development

Uterine preparation

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221
Q

What occurs to LH and FSH levels in the follicular phase of the menstrual cycle?

A

Oestrogen and progesterone are both low so FSH and LH can increase.
FSH causes maturation of several antral follicles.
Development of theca interna and LH stimulates cells to release oestrogen so oestrogen levels rise.
Oestrogen peak exerts positive feedback, especially on LH.
LH levels rise and stimulate ovulation.
Rising oestrogen levels also can proliferation of endometrial basal cells and glandular formation and formation of thin, alkaline cervical mucus.

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222
Q

What can the luteal phase of the menstrual cycle be further subdivided into?

A

Secretory phase days 25-22

Late secretory phase days 23-28

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223
Q

What are the main purposes of the luteal phase of the menstrual cycle?

A

Ovulation
provide brief period of fertility
Develop corpus luteum
Waiting phase

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224
Q

What happens in the ovary during the luteal phase of the menstrual cycle?

A

LH acts on granulosa cells to reorganise to form corpus luteum.
Luteal cells secrete oestrogen and progesterone.
Waiting phase for hCG secretion in the event of a pregnancy
If there’s no pregnancy, LH and FSH levels fall too much to be able to maintain corpus luteum so it degnerates into corpus albicans.
When corpus luteum degenerates, no longer progesterone and oestrogen secretion so LH and FSH can rise again

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225
Q

What happens to the endometrium during the luteal phase of the menstrual cycle?

A

After ovulation, progesterone stimulates the differentiation of the endometrium so there’s storage of nutrients, glands prepare for secretion and the endometrium thickens further.
Glands then start to secrete a glycogen rich milk in preparation for implantation
As progesterone and oestrogen levels fall, spiral arteries of functional layer necrose and blood leaks from these vessels and the whole of the functional layer is shed.

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226
Q

What would be the effect of hyperprolactinaemia be on fertility?

A

Would suppress fertility as prolactin disturbs the pulsatile release of GnRH

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227
Q

In what order do puberty events occur in females

A
Thelarche (breast buds)
Adrenarche (pubic hair)
Growth spurt
Menarche (periods)
Adult breasts
Adult pubic hair
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228
Q

What are the stages of thelarche?

A

Breast bud development
Juvenile smooth contour
Areola and papilla project above the breast
Adult breasts

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229
Q

What are the stages of adrenarche in females?

A

Sparse pigmented, long straight hair forms, mostly along labia
Hair becomes darker, more coarse and thicker
Hair fills out towards adult distribution

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230
Q

What hormone drives the closure of epiphyseal plates in females?

A

Oestrogen

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231
Q

When do menstrual cycles become ovulatory?

A

Roughly 10 months after menarche onset

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232
Q

What are the stages of puberty in males?

A
Spermatogenesis begins
Genital development
Adrenarche
Growth spurt
Adult genitalia
Adult pubic hair
Adult height
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233
Q

What are the main stages of genital development in males?

A
1-preadolescent
Lengthening of penis
Increase in length and circumference
Development of glans penis and darkening of scrotal skin
Adult genitalia
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234
Q

How is adrenarche in males different to in females?

A

Same except initial hair growth is around base of penis, rather than labia

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235
Q

What drives the onset of puberty?

A

Driven by brain and increase in GnRH causing increased secretion of LH and FSH. May occur due to decreased sensitivity to negative feedback of steroids or may be because of maturation of central mechanisms

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236
Q

What hormones drive adrenarche?

A

Androgens. Testosterone in males and androgens from adrenal glands in females

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237
Q

What hormone drives breast development?

A

Oestrogen

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238
Q

What hormones drive the growth spurt in puberty?

A

Growth hormone and sex steroids. Oestrogen causes earlier closure of epiphyseal plates.

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239
Q

What hormone drives male genital development?

A

Testosterone

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240
Q

What drives the initiation of menarche?

A

Thought to be related to weight. Needs roughly 47kg or equivalent proportion of eventual weight.

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241
Q

What is precocious puberty?

A

Signs of puberty at less than 8 years old

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242
Q

What may cause precocious puberty?

A

Neurological causes because of early stimulation of central mechanisms. May occur due to things like meningitis or melatonin secreting pineal tumours
Uncontrolled gonadotrophin/steroid hormone secretion due to hormone secreting tumours

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243
Q

Over what ages does thelarche normally occur?

A

Onset between 8-13

finishing at around 16

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244
Q

Over what ages does adrenarche normally occur in females?

A

Onset between 9 and 16. Normally ending around 16

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245
Q

Over what ages does growth spurt normally occur in females?

A

From around 10-15

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246
Q

Over what ages does menarche normally occur?

A

11-15. Average around 12.5

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247
Q

Over what ages does genital development occur in males?

A

Onset around 10-14

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248
Q

Over what ages does adrenarche occur in males?

A

Onset around 10-14

Last stage around 16

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249
Q

Over what age does spermatogenesis and testicular volume develop?

A

Starts between 9-13. Final stage around 12-16

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250
Q

Over what ages does growth spurt normally occur in males?

A

Around 12-17

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251
Q

When does menopause normally occur?

A

Between ages of 40-55 with average being 52. Lasts around 2-8 years

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252
Q

What happens in the pre-menopausal stage?

A

Changes to the menstrual cycle. Follicular phase decreases in length so ovulation occurs earlier or not at all. There’s falling oestrogen so LH and FSH start to rise.

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253
Q

What happens during the menopause?

A

Cessation of menstrual cycles. There are no new follicles to develop so there’s a dramatic fall in oestrogen. This means that LH increases and FSH dramatically increases.

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254
Q

What are the effects of the menopause?

A
Vascular changes leading to hot flushes
Collagen loss leading to reduced skin and bladder tone.
Regression of endometrium and shrinkage of myometrium
Thinning of cervix
Loss of vaginal rugae
Involution of breast tissue
Decreased bone mass 
Decreased libido
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255
Q

At what rate is bone mass lost in the menopause?

A

Roughly 2.5% per year

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256
Q

What does hormone replacement therapy involve?

A

Replacing oestrogens to treat menopausal symptoms and prevent long term effects. Can also use progesterone to prevent endometrial hyperplasia and carcinoma

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257
Q

What are some advantages of hormone replacement therapy?

A

Easy to administer
Relieves menopausal symptoms
Increases well being
Can limit osteoporosis

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258
Q

What are some disadvantages of hormone replacement therapy?

A

Not firstline treatment for osteoporosis
Can increase risk of breast cancer
Increase risk of DVT due to increased coagulability of blood.
Increased risk of cardiovascular disease

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259
Q

What is amenorrhoea?

A

The lack of periods

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260
Q

What are the different types of amenorrhoea and how are they defined?

A

Primary - either lack of periods with presence of secondary sexual characteristics at 16 years or lack of periods and lack of secondary sexual characteristics at 14 years
Secondary - Ceasing of menstruation. If a history of regular cycles then no periods for more than 3 months. If a history of irregular cycles then no periods for more than 9 months

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261
Q

What is menorrhagia?

A

Excessively heavy periods lasting for more than 7 days

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262
Q

What is dysmenorrhoea?

A

Painful periods

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263
Q

What is oligomenorrhoea?

A

Periods that occur at intervals of more than 35 days

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264
Q

What is premenstrual sysndrome?

A

Recurrent symptoms that occur in the last half of the menstrual cycle

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265
Q

What are the 3 main origins of amenorrhoea?

A

Outflow tract
Gonadal/end organ
Pituitary and hypothalamic/ central regulatory disorders

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266
Q

What hormone changes are there in outflow tract causes of amenorrhoea?

A

Should be none. HPG axis is still functional

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267
Q

What are some outflow tract causes of primary amenorrhoea?

A

Mullerian agenesis
Imperforate hymen
Vaginal atresia
Cryptomenorrhoea

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268
Q

What is cryptomenorrhoea?

A

Experience of cyclic menstrual pain but with apparent amenorrhoea

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269
Q

What’s an outflow tract cause of secondary amenorrhoea?

A

Intrauterine adhesions or scarring, ie asherman’s syndrome

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270
Q

What is asherman’s syndrome?

A

Fibrosis of the endometrium. Often due to surgical trauma

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271
Q

What hormonal changes are seen in end organ causes of amenorrhoea?

A

Ovaries are unresponsive to pituitary stimulation so there’s low oestrogen that may need treatment, and high fsh.
May need chromosomal testing if hypergonadotrophic in young individuals

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272
Q

What are some gonadal/end organ disorders that cause primary amenorrhoea?

A

Gonadal dysgenesis, ie in turner’s
Androgen insensitivity syndrome
LH/FSH receptor abnormalities
Congenital adrenal hyperplasia

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273
Q

What are some gonadal/end organ disorders that cause secondary amenorrhoea?

A
Polycystic ovarian syndrome
Pregnancy
Anovulation
Menopause
Premature menopause
Drug induced
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274
Q

What hormone changes are seen in central regulatory disorders that cause amenorrhoea?

A

Insufficient FSH so ovaries aren’t stimulated to produce enough oestrogen for menses to occur.

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275
Q

What’s a central regulatory cause of primary amenorrhoea?

A

Kallmann syndrome which is a disrupted interaction between the hypothalamus and pituitary gland that only affects LH and FSH

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276
Q

What are some central regulatory causes of secondary amenorrhoea?

A
Exercise amenorrhoea
Stress amenorrhoea
Eating disorders
Weight loss
Sheehan syndrome
Hyperprolactinaemia
Haemochromatosis
Hyper-/Hypoparathyroidism
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277
Q

How should secondary amenorrhoea be evaluated?

A
Menstrual history
Contraception use
Surgical history
Pregnancy
Weight changes
Medication
Chronic disease
Stress levels
Diet
Family history of menopause age, thyroid dysfunction, diabetes, cancer
Physcial exam looking at BMI, hair distribution, thyroid, visual field, breast discharge, abdominal masses/tenderness
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278
Q

Why should visual field be assessed when assessing secondary amenorrhoea?

A

As visual field changes are one of the first symptoms of a pituitary tumour

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279
Q

How should amenorrhoea be managed?

A

Take good history
Rule out pregnancy
Do blood tests for:
TSH, prolactin, LH and FSH if it’s an ovarian axis problem
LFTs in chronic disease
Testosterone, androgens and progesterone in presence of hirsuitism
MRI is CNS problem is indicated

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280
Q

When is a menstrual cycle indicated to be anovulatory?

A

If there’s oligomenorrhoea or amenorrhoea, with or without menorrhagia

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281
Q

What is dysfunctional uterine bleeding?

A

Excessively heavy, prolonged or frequent bleeding of uterine origin that’s not due to pregnancy, pelvic or systemic disease. Tends to be a diagnosis of exclusion and is anovulatory

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282
Q

When does dysfunctional uterine bleeding tend to occur?

A

At extremes of reproductive life and in women with polycystic ovarian syndrome

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283
Q

Why does dysfunctional uterine bleeding occur?

A

Due to a disturbance in the HPG axis so there’s a change in menstrual cycle length. There’s no withdrawal of progesterone from the endometrium so the endometrium builds up and there’s then erratic bleeding as the endometrium breaks down.

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284
Q

How is dysfunctional uterine bleeding managed?

A

Do coagulation workup
Measure TSH and HCG levels
Consider smear test
Can give oestrogen therapy

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285
Q

Why does menorrhagia most often occur?

A

Secondary to a distortion of the uterine cavity whereby the uterus is unable to contract the venous sinuses of the zona basalis. This causes heavy bleeding that may be prolonged.

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286
Q

What are some general categories of causes of menorrhagia?

A

Organic
Endocrine
Iatrogenic
Haemostatic

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287
Q

How should menorrhagia be managed?

A

Full history
FBC
Physical exam for anaemia, obesity. androgen excess, thyroid, liver, spleen, pelvic/uterine causes, cervix, adnexal
Treat with COCP or NSAIDs and long acting progestogens

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288
Q

What is true precocious puberty?

A

Onset of puberty due to premature secretion of gonadotrophins. Before age 6/7 depending on ethnicity in girls and before 9 in boys

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289
Q

What may be causing primary amenorrhoea if LH and FSH levels are normal?

A

Tissues aren’t responding to steroids.
Outflow tract problem
Androgen insensitivity syndrome

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290
Q

What is androgen insensitivity syndrome?

A

Occurs in XY males who are insensitive to tesosterone. Develop some secondary sexual characterisitics of female so normally present with amenorrhoea. There’s female external genitalia but not internal genitalia due to presence of MIH

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291
Q

What may be causing primary amenorrhoea if LH and FSH levels are low?

A

Pituitary/hypothalamic problem.

May be anorexia nervosa/nutrition

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292
Q

How is puberty stage assessed?

A

Checking height, weight, body hair, genitalia and bone age

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293
Q

What is delayed puberty?

A

Lack of sexual maturation by 15 years

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294
Q

What is the most common cause of delayed puberty?

A

Constitutional delay. Benign representation of normal variation. Will eventually undergo normal puberty. Mostly familial
May be due to serious systemic disease

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295
Q

How can bone age be assessed?

A

Taking hand-wrist films and comparing them with standards for the subject’s chronological age

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296
Q

What is the average rate of growth spurt in males?

A

10cm per year

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297
Q

How can cause of delayed puberty in males be distinguished

A

If bone age is less than chronological age, is constitutional delay.
If FSH is low, pituitary/hypothalamus problem
If testosterone is low - hypogonadism

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298
Q

What is precocious pseudopuberty?

A

The apparent onset of puberty with virilisation but no sperm production. Due to androgen secretion from adrenals or testes

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299
Q

What can cause precocious pseudopuberty?

A

Andrenal hyperfunction ie due to congenital adrenal hyperplasia
Adrenocortical tumour

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300
Q

How can the causes of precocious pseudopuberty be differentiated between?

A

Imaging to detect tumour

Enzyme testing for enzyme that’s elevated in congenital adrenal hyperplasia

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301
Q

What are some effects of oestrogen depletion in the menopause?

A
Hot flushes
disturbed sleep
Breast atrophy
Mood changes
Vaginal/urethral atrophy
Osteoporosis
Changing cholesterol/lipid profile
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302
Q

What are fibroids?

A

Benign, hormone dependent tumours of smooth muscle in the myometrium

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303
Q

How may fibroids be diagnosed?

A

Mostly asymptomatic
May present with menorrhagia
Can be palpable if very large by bimanual examination as an irregularly shaped uterus
Mass can be visualised on ultrasound but can’t differentiate between that and ovarian tumours

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304
Q

What constitutes as excessive menstrual blood loss?

A

More than 80 ml. Enough to cause anaemia

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305
Q

How can menorrhagia extent be assessed?

A

Pad/tampon count

Haematocrit/haemoglobin count

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306
Q

How can fibroids be treated?

A

Depends on patient’s age, symptoms and desire for fertility. If she’s close to menopause, should regress in absence of steroid hormones
Can treat with a GnRH agonist
Remove by endoscopic resection
Do abdominal myomectomoy/hysterectomy

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307
Q

Evaluate the removal of ovaries alongside uterus?

A

Avoid future ovarian pathology but ovarian type tumours can arise from the peritoneum de novo
WIll also cause sudden menopause onset

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308
Q

What is the scrotum?

A

A fibromuscular extension of the perineum that holds the testes, epididymis and first part of spermatic cord.

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309
Q

What is the embryonic origin of the scrotum?

A

Genital folds

310
Q

What is a remnant of the scrotum’s embryonic origin?

A

The midline scrotal raphe that’s continuous with the ventral penile raphe

311
Q

Where is the scrotum?

A

Posteroinferior to the penis and inferior to the pubic symphysis

312
Q

What lies deep to the scrotal raphe?

A

Septum of scrotum that divides the scrotum in two

313
Q

What is the arterial supply to the scrotum?

A

Anterior and posterior scrotal arteries

314
Q

What is the lymphatic drainage of the scrotum?

A

To superficial inguinal nodes

315
Q

What is the nervous supply to the scrotum?

A

Scrotal nerve

316
Q

What is the difference in distribution between the parietal and visceral tunica vaginalis in males?

A

Parietal is more extensive and extends superiorly into the distal spermatic cord

317
Q

What forms the mediastinum of the testis?

A

A posterior thickening of the tunica albuginea

318
Q

What is the blood supply to the testes?

A

Testicular arteries which arise directly from the abdominal aorta

319
Q

What is the venous drainage of the testes?

A

Right testis drains to pampiniform venous plexus then to right testicular vein then into the inferior vena cava
Left testis drains to pampiniform plexus then to left testicular vein, then to left renal vein before joining the inferior vena cava

320
Q

What is the lymphatic drainage of the testes?

A

Drains to paraaortic nodes

321
Q

Where is the epididymis?

A

On the superior and posterolateral surface of the testis

322
Q

What are the main functions of the epididymis?

A

Storage of sperm
Maturation of sperm so they gain structural maturation and motility
Sperm transport

323
Q

What are the 3 main parts of the epididymis?

A

Head formed by convergence of ductus efferentes of the rete testis
Body which is a single highly convuluted tubule
Tail which is an area of transition between the epididymis and vas deferens

324
Q

What is the vas deferens?

A

A straight, muscular tube that emerges from the tail of the epididymis to transport sperm

325
Q

What route does the vas deferens take?

A

Enters spermatic duct, travels along pelvic side wall and then between the bladder and ureter, combines with seminal vesicles to form the ejaculatory duct

326
Q

What does the spermatic cord contain?

A
Vas deferens
Testicular artery
Cremasteric artery
Pampiniform plexus
Artery to vas deferens 
Genital branch of genitofemoral nerve
Lymphatics
Processus vaginalis
327
Q

What path does the spermatic cord take to exit the abdomen?

A

Through the deep inguinal ring, lateral to the inferior epigastric vessels (pulling fascial coverings with it) (same route as indirect inguinal hernias) Then through the inguinal canal and into the scrotum at the posterior border of the testis

328
Q

What are the coverings of the spermatic cord, deep to superficial?

A

Internal spermatic fascia, formed from transversalis fascia
Cremasteric muscle and fascia, from transversalis and internal oblique
External spermatic fascia, from aponeurosis of external oblique

329
Q

What is the pampiniform plexus?

A

A network of small veins that surrounds the testicular arteries and so acts as a heat exchanger to reduce the temperature of the testis to maximaise spermatogenesis

330
Q

What is the distribution of nerves from the lumbar and sacral plexuses to the testes and scrotum?

A

Lumbar plexus supplies the anterior surface of the testes and scrotum
Sacral plexus supplies the posterior and inferior surfaces

331
Q

Where do the seminal vesicles lie?

A

Between the bladder and the rectum

332
Q

What is within the lumen of the seminal vesicles?

A

Mucous membrane is highly folded so that it projects into the lumen. Lumen holds coagulated secretion

333
Q

What are the main anatomical relationships of the prostate gland?

A
Inferiolateral - Levator ani
Posterior - ampulla of rectum
Base - Neck of bladder
Apex - urethral sphincter and deep perineal muscles
Muscular anterior - urethral sphincter
334
Q

What is the lymphatic drainage of the prostate gland?

A

Mostly by internal iliac nodes but can also be via sacral

335
Q

What’s the internal erectile structure of the penis?

A

A pair of corpora cavernosa dorsally
Single corpora spongiosum ventrally (holds urethra)
These are a netwrok of fibromuscular tissue with spaces that can become filled with blood during an erection

336
Q

What is the arterial supply to the penis?

A

Internal pudendal artery via anterior division of internal iliac artery

337
Q

What is the venous drainage of the penis?

A

venous plexus to deep dorsal vein of penis to prostatic venous plexus to internal iliac vein to inferior vena cava

338
Q

What does the control of erection depend on?

A

Adequate neurological regulation
Adequate arterial flow
Functioning venous drainage

339
Q

Which two muscles of the perineum help to maintain erections?

A

Bulbospongiosus

Ischiocavernosus (compresses veins)

340
Q

What is a hydrocoele?

A

A build up of serous fluid in the tunica vaginalis

341
Q

What is a haematocoele?

A

Build up of blood in the tunica vaginalis

342
Q

How can a haematocoele and a hyrdocoele be differentiated between clinically?

A

By transillumination. Haematocoele will appear more red

343
Q

What is a varicocoele?

A

A varicosity of the paminiform plexus

344
Q

Why are varicocoeles more common on the left?

A

Due to the angle at which the left testicular vein enters the left renal vein
Lack of effective valves between testicular and renal vein
Increased reflux from compression of the renal vein

345
Q

What is a spermatocoele?

A

A retention cyst containing spermatogonia in the epididymis

346
Q

What is oligozoospermia?

A

A condition where there’s abnormally low numbers of spermatozoa in the semen

347
Q

What is azoospermia?

A

Condition where no sperm is found in the ejaculate

348
Q

What are cryptorchid testicles?

A

Undescended testicles.

349
Q

Why do undescended testicles impar spermatogenesis?

A

Subject to increased temperature. Sertoli and leydig cells still secrete male sex hormones but spermatogenesis can’t take place

350
Q

What is orchitis?

A

Inflammation of the testes. Impairs spermatogenesis and may be seminiferous tubule degeneration and infertility

351
Q

What can lead to an absence of germ cells and so azoospermia?

A

Drugs
Viral infections
Irradiation

352
Q

What is a relatively common cause of orchitis?

A

Mumps infection in puberty

353
Q

Where do indirect inguinal hernias enter the inguinal area?

A

Indirectly so through the inguinal canal, lateral to the inferior epigastric vessels, along the route of the spermatic cord.

354
Q

What is testicular torsion?

A

A twisting of the spermatic cord, usually just superior to the upper pole of the testis, putting the testis at risk of necrosis

355
Q

What are the main symptoms of benign prostatis hyperplasia?

A

Dysuria
Nocturia
Frequency

356
Q

How do prostatic malignancies metastasise?

A

In blood to internal vertebral plexus and so to vertebrae and bones
Through lymphatics in internal iliac and sacral nodes

357
Q

What makes up the pelvic girdle?

A

Right and left hip bones, sacrum and coccyx

358
Q

What are the features of a good pelvis for childbirth?

A
Gynecoid
Round pelvic inlet
Straight side walls
Subpubic arch more that 80 degrees
Non-prominent ischial spines
Well rounded greater sciatic notch (roughly 90 degrees)
Well curved sacrum
359
Q

What are the typical features of a male pelvis?

A
Android
Heart shaped inlet
Funnel shaped side walls
Subpubic arch less than 70 degrees
Prominent ischial spines
Narrow greater sciatic notch (roughly 70 degrees)
Less curved sacrum
360
Q

What is the pelvic inlet?

A

Circular opening between the abdominal and pelvic cavities. Where structures pass between these cavities. Completely surrounded by bones and joints

361
Q

What are the different components of the pelvic inlet?

A
Sacral promontory
Margin of ala
Arcuate line
Pecten pubis
Pubic crest
Arcuate line + pecten pubis + pubic crest is the linea terminalis
362
Q

What is the pelvic outlet?

A

Diamond shaped opening though which the terminal parts of the GI, urinary and reproductive tracts pass.

363
Q

What are the main components of the pelvic inlet?

A

Pubic arch made up of pubic and ischial rami, inferior body of pubis and ischial tuberosity
Sacrotuberous ligament

364
Q

What is the greater pelvis made up of?

A

False pelvis of no obstetric relevance. Includes whole pelvis

365
Q

What is the lesser pelvis?

A

True pelvis. Consists of pelvic inlet and pelvic outlet but not the bones and landmarks outside of these

366
Q

What are some measurements done to assess the anteroposterior diameter of the pelvic inlet?

A

Anatomic conjugate - measure from sacral promontory to the top of the pubic symphysis
Obstetric conjugate - from promontory to midpoint of pubic symphysis
Diagonal conjugate - from promontory to bottom of pubic symphysis

367
Q

What assessments can be done of the midpelvis before birth?

A

Check if pelvic side walls are straight

Measure bispinous diameter - between ischial spines

368
Q

What assessments can be done of the pelvic outlet before birth?

A

Infrapubic angle

Distance between ischial tuberosities

369
Q

What helps to increase the mobility of the testes in the scrotum?

A

A fluid layer within the cavity of tunica vaginalis

370
Q

What is the cremasteric reflex?

A

Sinal reflex arc whereby stroking the superomedial thigh, innervated by the ilioinguinal nerve (L1) stimulates the genital branch of the genitofemoral nerve (L1-L2) to contract thecremaste rmuscle which elevates the ipsilateral testis

371
Q

How is the testis protected from the cold?

A

Dartos muscle is within the wall of the scrotum and gets sympathetic innervation from the genitofemoral nerve. Cold temperatures cause contraction of the dartos muscle and this wrinkles the scrotal skin, reducing the surface area available for heat loss.

372
Q

How can testicular cancer spread to cervical lymph nodes?

A

Testes are drainedvia spermatic cords to the paraaortic nodes. These anastamose with the intrathoracic nodes and then with the cervical lymph nodes.

373
Q

What is the path of the vas deferens?

A

Tail of epididymis - inguinal canal - pelvic side wall - ejaculatory duct - prostatic urethra

374
Q

What is cut in a vasectomy?

A

Vas deferens are ligated bilaterally from the superoanterior scrotal wall.

375
Q

What is the effect of a vasectomy?

A

Sperm degenerates in the epididymis and proximal ductus deferens and then debris is removed by phagocytosis. Therefore ejaculate is only composed of secretions from seminal vesicles and the prostate gland

376
Q

What are the anatomical landmarks passed during the descent of the testis and by which foetal month are they reached?

A

Iliac fossa by month 3
Inguinal canal by month 7
External ring by month 8
Scrotum by month 9

377
Q

What controls the contraction of smooth muscle in ejaculation?

A

Sympathetic hypogastric nerve (L1-L2)

378
Q

What do seminal vesicles secrete and for what purpose?

A

Fructose - provides ATP by sperm
Prostaglandins - facilitate sperm motility
Clotting factors eg semenogelin to coagulate sperm

379
Q

What does the prostate gland secrete and for what purpose?

A

Citric acid - provides ATP for sperm in krebs cycle
Proteolytic enzymes - re-liquefies sperm
Acid phosphatase

380
Q

What do bulbourethral glands secrete and for what purpose?

A

Alkaline fluid to neutralise urethra and female reproductive tract
Mucus to lubricate end of penis and urethral lining

381
Q

What is the arterial supply to the prostate gland?

A

Inferior vesical artery (from internal iliac)

382
Q

WHy is the membranous part of the urethra relatively indistensible?

A

As it’s surrounded by sphincter urethrae muscle and the perineal membrane

383
Q

What is the blood supply to the penis?

A

Deep arteries and dorsal arteries supply corpora cavernosa and crura of penis
Dorsal arteries and arteries of the bulb supply corpora spongiosum and bulb of penis

384
Q

What is the crura of the penis?

A

Continuation of the corpora cavernosa that attaches to the pubic arch

385
Q

What changes in blood flow help maintenance of an erection?

A

Vasodilation of arterioles to corpora cavernosa and subsequent increased blood flow causes venous engorgement. The tunica albuginea and fascial sheaths resist any potential engorgement so internal pressure rises and venous return in occluded.
Normally, blood from cavernous spaces drains to venous plexuses and then into deep dorsal vein but this is compressed so rigidity is maintained.
Venous return is further obstructed by bulbospongiosus and ischiocavernosus muscles.

386
Q

Why is the corpus spongiosum not rigid in erection?

A

It swells with blood but its surrounding tunica albuginea isn’t as fibrous or restrictive so venous return isn’t as obstructed. High ressure due to rigidity would compress the urethra and so prevent ejaculation

387
Q

What normally prevents retrograde ejaculation into the bladder?

A

Closure of the neck of the bladder in ejaculation

388
Q

What carries afferent information from the glans penis?

A

Pudendal nerve (S2-S4)

389
Q

What’s the efferent outflow to penis in erection, emission and depression of erection?

A

Erection is parasympathetic via pelvic nerve (S2-S4) due to smooth muscle relaxation of coiled arteries
Emission is sympathetic from L1-L2
Depression is parasympathetic from hypogastric nerve (T10-L2) causing increased myogenic tone in arterial smooth muscle

390
Q

What are some possible causes of erectile dysfunction?

A

Psychological
Tear in fibrous capsule of corpora cavernosa
Obstruction of blood flow to corpora cavernosa
Pharmacological

391
Q

Why is the obstetric conjugate the most relevant AP diameter of the pelvic inlet?

A

Is the narrowed point of the AP aspect

392
Q

What is the normal length of the obstetric conjugate?

A

Ideally around 10 cm

393
Q

How is the diagonal conjugate measured clinically?

A

Inserting 2 fingers into the vagina and feeling for the sacral promontory then noting the position of the under edge of the pubis on ones hand

394
Q

What is the ideal length of the diagonal conjugate?

A

11.5cm

395
Q

Why may hydrocoeles grow on coughing, in young boys?

A

Tunica vaginalis still continuous with peritoneum so increasing intrabdominal pressure can push through more intraperitoneal fluid and so the hydrocoele increases in size

396
Q

How can an epididymal cyst and a spermatocoele be distinguished between?

A

By transillumination. Epididymal cyst transilluminates very well but the contents of spermatocoele is turbis and so inhibits transillumination

397
Q

What does the gubernaculum turn into?

A

Round ligament and superior part becomes ovarian ligament

398
Q

What is the mesovarium an extension of?

A

Posterior extension of the broad ligament

399
Q

What does the mesovarium do?

A

Surrounds and suspends the ovaries

400
Q

What is the arterial supply to the ovaries?

A

Ovarian arteries that come directly off the aorta

401
Q

What is the venous drainage of the ovaries?

A

Left ovarian vein goes to left renal vein then IVC

Right ovarian vein drains directly into IVC

402
Q

What is the lymphatic drainage of the ovaries?

A

Paraortic nodes

403
Q

What is the position of the uterus in relation to the cervix and vagina?

A

Anteverted on the vagina

Anteflexed on the cervix

404
Q

What is the broad ligament?

A

Mesentery extending from sides of the uterus to the lateral walls and the floor of the pelvis. Made of mesentery of uterus, fallopian tubes and ovaries

405
Q

What is the purpose of the broad ligament?

A

Assists with keeping the uterus in position

406
Q

What is the round ligament?

A

Remnant of the gubernaculum. Travels from horns of the uterus, through the inguinal canal and attaches to the labia majora (labioscrotal folds) Also attached to the ovaries.

407
Q

What is the name of the funnel shaped opening of the fallopian tubes?

A

Ostium

408
Q

What is the position of the fallopian tubes in relation to the ovaries?

A

Pass superiorly over the ovaries and then terminate laterally to thm

409
Q

What is the position of the cervix in relation to the vagina?

A

Anteverted on the vagina

410
Q

What is the purpose of the cervix?

A

To allow sperm to enter the uterine cavity from the vagina

Protect the genital tract from bacterial invasion

411
Q

What is the transverse cervical ligament?

A

Thickening at the base of the broad ligament that gives lateral stability to the cervix

412
Q

What is the uterosacral ligament?

A

Attaches cervix to the sacrumto oppose the anterior pull of the round ligament and so assist in maintaining the natural anteversion of the cervix

413
Q

What is the blood supply to the uterus?

A

Uterine artery which passes superior to the ureters Comes off the anterior division of the internal iliac artery

414
Q

What is the venous drainage of the uterus?

A

Uterine venous plexus drains to uterine veins which drains to internal iliac vein, common iliac vein and then IVC

415
Q

What’s the lymphatic drainage of the different parts of the uterus?

A

Fundus drains to aortic nodes
Body to external iliac nodes
Cervix to external and internal iliac nodes and sacral nodes

416
Q

What is the vaginal vault?

A

An internal enlargement of the vaginal canal, where semen is deposited.

417
Q

Where is the vagina in relation to the urethra?

A

Urethra is fused to the anterior vaginal wall

418
Q

What is the name of the exteror opening of the vagina?

A

Introitus

419
Q

In what direction does the vagina pass through the pelvic cavity?

A

Posterosuperiorly

420
Q

What are the 3 layers of the vaginal wall?

A

Mucous membrane lined by stratified squamous epithelium
Muscular coat of longitudinal and circular smooth muscle layers
Fibrous adventitia

421
Q

What is the blood supply to the vagina?

A

Upper part is supplied by uterine arteries
Lower and middle parts are supplied by vaginal and internal pudendal arteries. Pudendal artery comes off the anterior division of the iliac artery. Vaginal artery comes off the uterine artery

422
Q

Where is the vaginal venous plexus?

A

Along the sides of the vaginal wall, within the mucosa

423
Q

What does the vaginal venous plexus communicate with?

A

Vesical and rectal venous plexuses

424
Q

What is the venous drainage of the vagina?

A

Vaginal plexus to vaginal vein the uterine vein to internal iliac vein

425
Q

What is the innervation of the vagina?

A

Inferior fifth gets somatic innervation from pudendal nerve

Superior 4/5 of the vagina and uterus gets innervation from the uterovaginal plexus from the prevertebral chain

426
Q

What is the nerve roots of the pudendal nerve

A

S2-S4

427
Q

What is pain the vagina detected by?

A

Depends where pain is in relation to the pelvic pain line. If above the pain line, follows sympathetic fibres to inferior thoracic and superior lumbar spinal ganglia
If below the pain line, detected by spinal ganglia of S2-S4

428
Q

Where is the pelvic pain line?

A

Corresponds to the inferior limit of the perineum

429
Q

What does the vaginal vestibule contain?

A

Vagina, urethra and greater and lesser vestibular glands

430
Q

What are the lesser vestibular glands?

A

Also called Skene’s glands. Homologous with prostrate gland in male

431
Q

What are the greater vestibular glands?

A

Bartholin’s glands. Homologous with bulbourethral glands in male. Secrete mucus

432
Q

How many ovarian cysts are needed to be classed as PCOS?

A

More than 10

433
Q

What is salpingitis?

A

Inflammation of the uterine tube which can cause fusion or adhesions, blocking the lumen and so causing infertility

434
Q

What are some symptoms of salpingitis?

A
Abnormal vaginal discharge
Pain of ovulation
Pain on sex
Pain on and off through periods
Back pain
Abdominal pain
Fever
Nausea and vomiting
Bloating
435
Q

How can a bimanual examination help to diagnose pelvic inflammatory disease?

A

Can isolate cervix and test for cervical motion tenderness which is a sign of PID

436
Q

What causes vaginisimus?

A

Reflex of pubococcygeus. May have psychological origins

437
Q

What are the two main holes within the pelvic floor?

A

Urogenital hiatus anteriorly to allow passage of urethra and vagina
Rectal hiatus centrally

438
Q

What are the purposes of the pelvic floor muscles?

A

Support of abdominopelvic viscera through tonic contraction
Urinary and faecal incontinence through sphinceter action
Resistance to raised intra abdominal/ intrapelvic ressure

439
Q

What are the three components of the pelvic floor?

A

Levator ani muscles
Coccygeus muscle
Fascia surrounding muscles

440
Q

What’s the nerve supply to the levator ani muscles?

A

Pudendal nerve. Branches s2-s4

441
Q

What are the 3 levator ani muscles?

A

Puborectalis
Pubococcygeus
Iliococcygeus

442
Q

What are the attachments of the levator ani muscles?

A

Anteriorly - Bodies of pubic bones
Laterally - Thickening of fascia of obturator internus, called tendinous arch
Posteriorly - ischial spines

443
Q

Where does puborectalis muscle run?

A

From pubic bodies, past the urogenital hiatus and around the anal canal

444
Q

What is the function of puborectalis?

A

Bends anal canal anteriorly, creating the 90 degree angle between the rectum and anus
Maintains faecal incontinence so relaxes in defecation

445
Q

Where does pubococcygeus run?

A

From bodies of pubic bones and anterior aspect of tendinous arch, travel around the urogenital hiatus to then attach at the coccyx and anococcygeal ligament
Some fibres also loop round to surround the prostate - levator prostatae or vagina - pubovaginalis

446
Q

Where does the iliococcygeus run?

A

From ischial spines posterior aspect of tendinous arch to the coccyx and anococcygeal ligament

447
Q

What is the coccygeus muscle innervated by?

A

Anterior rami of S4, S5

448
Q

Where does coccygeus muscle run from?

A

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

449
Q

What is the purpose of the levator ani muscles in childbirth?

A

Support the foetal head during cervical dilation

450
Q

What are some risk factors for pelvic viscera prolapse?

A
Age
Number of vaginal deliveries
Family history
Chronic cough
Weight
451
Q

What are the anatomical borders of the perineum?

A
Anterior - Pubic symphysis
Posterior - Coccyx
Lateral - inferior pubic and ischial rami and sacrotuberous ligament
Roof - pelvic floor
base - Skin and fascia
452
Q

What are the surface borders of the perineum?

A

Anterior - Mons pubis/base of penis
Laterally - medial surfaces of thighs
Posterior - superior end of intergluteal cleft

453
Q

How can the perineum be further subdivided?

A

By drawing a line transversely between the ischial tuberosities to give the anterior urogenital triangle and th posterior anal triangle

454
Q

What’s contained in the anal triangle?

A

Anal aperture
External anal sphincter muscle
Two ischioanal fossae that contain fat and connective tissue to aid with the expansion of the anal canal on defecation

455
Q

How is the anterior urogenital triangle further subdivided?

A

By perineal membrane. This forms a superficial and deep perineal pouch

456
Q

What is contained within the deep perineal pouch?

A

Part of the urethra and the external urethral sphincter. In males contains bulbourethral glands and deep transverse perineal muscles

457
Q

What is contained in the superficial perineal pouch?

A
Erectile tissue
Ischiocavernosus
Bulbospongiosus
Superficial transverse perineal muscles
Bartholin's glands
458
Q

What are the muscles of the perineal body innervated by?

A

Pudendal nerve (S2-S4)

459
Q

What are the main muscles of the perineal body?

A

Ischiocavernosus
Bulbospongiosus
Superficial transverse perineal muscles

460
Q

What are some relatively common sites of ectopic pregnancy implantation?

A
Fimbriae
Ampulla
Isthmus
Interstitium
Ovary
461
Q

What are some rare sites for ectopic implantation?

A

Pouch of Douglas

Abdominal viscera

462
Q

What is bleeding in an ectopic pregnancy due to?

A

Withdrawal bleed from falling hCG hormone, normally maintaining corpus luteum

463
Q

What forms the broad ligament?

A

Reflection of the peritoneum off the body of the uterus

464
Q

How does cervical mucus change over the uterine cycle?

A

In follicular phase, produced in highest amounts. Changes from cloudy to clear. At ovulation, is clear with high level of stretchability
After ovulation, less is produced and becomes cloudier and stickier

465
Q

Where do nabothian cysts develop?

A

From cervical glandular ducts

466
Q

How can nabothian cysts affect fertility?

A

Make cervix inhospitable, especially if cysts become infected. This therefore reduced the chance of a pregnancy occurring.

467
Q

How is the bony pelvis assessed in early pregnancy?

A
Bimanual exam
Palpating ischial spines
Measuring intertuberous distance
Assessing subpubic arch
Assessing diagonal conjugate
468
Q

What can palpation of the posterior fornices help to evaluate?

A

Posterior funduc
Uterosacral ligaments
Posterior broad ligaments
Pouch of douglas

469
Q

What can palpation of the anterior fornices help to evaluate?

A

Bladder

Rectopubic space

470
Q

Why is it important for the foetal head to rotate after delivery?

A

To move the shoulders into the long axis of the pelvic outlet

471
Q

What muscles can be felt when anus is squeezed around examining finger on a DRE?

A

External anal sphincter

Puborectalis

472
Q

What needs to be repaired after an episiotomy?

A
Vaginal mucosa
Vaginal submucosa
Perineal skin
Perineal muscles
Perineal fascia
473
Q

What are the main sources of data on genital tract infections?

A

GUM clinics but this underestimates true incidence due to patients reporting to other services and majority of burden being asymptomatic
Communicable disease surveillance centres get regular aggregate data returns from GUM clinics and other settings/

474
Q

What may have caused the increase in diagnosis of STIs?

A

Increased transmission due to altered sexual and social behaviours
Increased attendance to GUM clinics
Greater public, practitioner and national awareness
Improved diagnostic methods
Increased use of screening methods

475
Q

What groups are at increased risk of contracting STIs?

A

Young people
People of ethnic minorities
Those subject to poverty and social exclusion
People from lower socioeconomic background
People with less educational opportunities
Unemployed people
Those born to teenage mothers

476
Q

What are some characteristics of sexual behaviour that increase the risk of contracting an STI?

A
Age at first sexual intercourse
Total number of sexual partners
Frequency of partner change
Concurrent partners
Sexual orientation
Practice of unsafe sex
Lack of skills and confidence to negotiate safer sex
477
Q

What are some morbidities that are associated with STIs?

A
Pelvic inflammatory disease
Reproductive tract cancers
Impaired fertility
Risk of infection with blood borne virus
Risk of congenital or peripartum infection of neonate
478
Q

What are some differential diagnoses of genital skin and mucous membrane lesions?

A

May be genital ulcers - due to HSV or syphillis
Vesicles/bullae- most probably due to HSV
Genital papules
Anogenital warts

479
Q

What are the main symptoms of urethritis?

A

Dysuria, frequency, discharge

480
Q

What are some possible causes of urethritis?

A

Gonococcal (more in men than women) due to neisseria gonorrhoea infection
Chlamydial
Post gonococcal
Nongonococcal, due to chlamydia, ureaplasma, mycoplasma, HSV or trichomas
Non-infectious

481
Q

What are the main symptoms of cervicitis and vulvovaginitis?

A
Itching
Odour
Discharge
Soreness
Dyspareunia
482
Q

What are the main causes of vulvovaginitis?

A
Candidiasis
Trichomoniasis
Staphylococcal
HSV
Foreign body
483
Q

What are the main causes of cervicitis?

A

Chlamydia
Gonorrhoea
HPV
HSV

484
Q

What is bartholinitis caused by?

A

Normally microbial infection by endogenous flora.

Rarely can be sexually transmitted

485
Q

What are some pregnancy related infections of the female pelvis?

A
Chorioamnionitis
Post partum endometriosis
Episiotomy infection
Osteomyelitis pubis
Ovarian vein thrombophlebitis
486
Q

What are the different classes of prostatitis?

A

Acute bacterial
Chronic bacterial
Chronic pelvic pain syndrome (no sign of UTI)

487
Q

What can orchitis be caused by?

A

Pyogenic bacterial by mumps infection of can be viral by coxsackie B

488
Q

What is chlamydia caused by?

A

Chlaymydia trachomatis (gram negative)

489
Q

How does chlamydial infection take hold in females?

A

Infect and replicates within cervical and urethral epithelium

490
Q

What are the symptoms of chlamydia in females?

A

Mostly asymptomatic.
Can cause cervicitis
Urethritis
If the infection ascends, however, can cause clinical/subclinical pelvic inflammatory disease presenting as salpingitis, endometritis or rarely, perihepatitis

491
Q

What are the symptoms of chlamydia in males?

A

Mostly urethritis

492
Q

What are some possible complications of chlamydia in males?

A
Acute epididymitis
Reiters syndrome (conjunctivitis, arthritis, urethritis)
493
Q

What are some neonatal complications of chlamydia?

A

Can cause neonatal conjunctivitis and neonatal pneumonia, if untreated

494
Q

How is chlamydia diagnosed?

A

Endocervical or urethral swab

First catch urine analysis followed by enzyme immunoassays, immunofluorescence and PCR

495
Q

How is chlamydia treated?

A

Doxycycline or a single, large dose of azithromycin

496
Q

What causes gonorrhoea?

A

Neisseria gonorrhoea - gram negative diplococci

497
Q

What symptoms are seen in gonorrhoea in females?

A

Acute cervicitis
Discharge
Urethritis

498
Q

What are some possible complications of gonorrhoea in females?

A

Bartholin’s gland abscess
Pelvic inflammatory disease
Disseminated gonococcal infection causing joint pain, rash and tenosynovitis

499
Q

What are some symptoms of gonorrhoea in males?

A

Urethritis
Prostatitis
Proctitis
Pharyngitis

500
Q

What are some possible complications of gonorrhoea in males?

A

Epididymitis

Disseminated gonococcal infection

501
Q

How is gonorrhoea diagnosed?

A

Urethral, endocervical, rectal and pharyngeal swabs which are then cultured

502
Q

How is gonorrhoea treated?

A

Single large oral dose of ciprofloxacin or intramuscular ceftriaxone
PLUS
7 day doxycycline (if co-chlamydial)
or
SIngle large oral dose of azithromycin if pregnant/compliance issues

503
Q

What is genital herpes caused by?

A

Herpes simplex virus which is encapsulated souble stranded DNA virus, of which there are 2 types

504
Q

What are the symptoms of primary genital herpes?

A

Extensive, painful, genital ulceration
Dysuria
Inguinal lymphadenopathy
Fever

505
Q

How is genital herpes diagnosed?

A

By taking a smear and swab from the vesicular fluid and/or of the ulcer base

506
Q

How is genital herpes treated?

A

With aciclovir

507
Q

What kind of virus is the human papilloma virus?

A

Double stranded DNA

508
Q

What is the presentation of genital warts?

A

Benign, painless, verrucours mucosal or epithelial outgrowths occuring at the penis, vulva, vagina, urethra, cervix or perineal skin

509
Q

How are genital warts diagnosed?

A

Either clinically or by biopsy with genome analysis

510
Q

How can genital warts be treated?

A

Topical podophyllin, cryotherapy or intralesional interferon

Can also spontaneously resolve

511
Q

What is syphilis caused by?

A

Treponema pallidum which is a spirocheate bacterium

512
Q

What are the stages of syphilis infection?

A

Stage 1 causes an indurated, panless ulcer or chancre
After 6-8 weeks, stage 2 causes lymphadenopathy, fever, rash and mucosal lesions
Can be latent years and stage 3 causes chronic granulomatous lesions
Stage 4 causes CVS and CNS complications

513
Q

How is syphilis diagnosed?

A

Dark field microscopy and serology

514
Q

What causes trichomonas vaginitis?

A

Trichomonas vaginalis flagellated protozoan

515
Q

What are the symptoms of trichomoniasis?

A

Thin, frothy, offensive discharge
Irritation
Dysuria
Vaginal inflammation

516
Q

How is trichomoniasis treated?

A

With metronidazole

517
Q

What are some risk factors for vulvovaginal candidiasis?

A
OCP
Antibiotics
Obesity
Steroids
Diabetes
Pregnancy
518
Q

What are the symptoms of candidiasis infection?

A

Profuse, white, curd like discharge
Vaginal Itching
Discomfort
Erythema

519
Q

How is candidiasis diagnosed?

A

High vaginal smear and culture

520
Q

How is candidiasis treated?

A

With topical azoles, nystatin or oral fluconazole

521
Q

What causes bacterial vaginosis?

A

Overgrowth of normal flora, particularly gardneralla

522
Q

What are the signs and symptoms of bacterial vaginosis?

A

Scanty but offensive fishy discharge

pH>4.5

523
Q

How is bacterial vaginosis diagnosed?

A

High vaginal smear. Will show ‘clue cells’ with are epithelia studded with gram negative coccobacilli, also with reduced lactobacilli and absence of neutrophils

524
Q

How is bacterial vaginosis treated?

A

With metronidazole

525
Q

What is pelvic inflammatory disease?

A

The result of an infection that rises from the endocervix causing salpingitis, endometritis, tuboovarian abscenn, parametritis, oophoritis and/or pelvic peritonitis

526
Q

What are some risk factors for pelvic inflammatory disease?

A
Sexual behaviour
Alcohol/drug use
Cigarette smoking
Contraception type
Being of lower socioeconomic background
Young people
527
Q

What bacteria cause pelvic inflammatory disease?

A

Primarily gonorrhoea and chlamydia with increased risk if these occur together
Also gardnerella, mycoplasma and anaerobes

528
Q

What effects do certain contraception types have on the risk of pelvic inflammatory disease?

A

Intrauterine coil gives an increased risk of pelvic inflammatory disease in the first few weeks after insertion
Combined oral contraceptive pill minimises symptoms but doesn’t reduce risk of infection

529
Q

What are the clinical features of pelvic inflammatory disease?

A

Pyrexia (>38)
Pain - can be bilateral abdominal tenderness, adnexal tenderness, cervical excitation, deep dyspareunia
Abnormal vaginal or cervical discharge

530
Q

What are the main differential diagnoses of pelvic inflammatory disease?

A
Ectopic pregnancy
Endometriosis
Complications of ovarian cyst
Irritable bowel syndrome
Appendicitis
UTI
Functional pain
531
Q

How is pelvic inflammatory disease investigated?

A

Triple swab - 2 endocervical for gonorrhoea and chlamydia. 1 deep vaginal for trichomonas vaginalis, bacterial vaginosis, candida

532
Q

When should hospital admittance for pelvic inflammatory disease be considered?

A
If disease is clinically severe
With a tuboovarian abscess
If surgical emergency can't be excluded
If there's lack of tolerance or response to oral therapy
If in pregnancy
533
Q

How is pelvic inflammatory disease treated?

A

analgesia
If mild, oral doxycycline and metronidazole and intramuscular ceftriaxone
If severe, IV doxycycline, ceftriaxone and metronidazole
Continue course fo 14 days

534
Q

When should a laparoscopy/laparotomy be considered in pelvic inflammatory disease?

A

If disease is clinically severe
In a tuboovarian abscess
If there’s no response to therapy

535
Q

What does a diagnosis of pelvic inflammatory disease put you at future increased risk of?

A

Ectopic pregnancy
Infertility
Chronic pelvic pain
Ftiz Hufh Curtis syndrome

536
Q

WHat is Fitz Hugh Curtis syndrome?

A

Adhesions of the liver causing RUQ pain and perihepatitis

537
Q

What are some important features of a sexual health history?

A
Recent sexual contact details 
If partners are symptomatic/have sought advice/treatment
Previous STIs/complications
Overseas travel and place of residence
Participation in commercial sex
Underlying diseases
Recent antibiotic use
Allergies
538
Q

Why does the COCP and pregnancy increase the risk of thrush?

A

Yeast overgrowht is favoured by high oestrogen levels

539
Q

How is thrush managed?

A

Withdraw or control risk factors
Only treat if particularly symptomatic then topical nystatin/azoles or oral fluconazole if problematic
Obtain high vaginal smear and sab for microscopy and culture
Consider treating partner to reduce frequency of re-transmission
If recurrent or unusually severe, investigate for resistant yeasts

540
Q

How is herpes simplex virus managed?

A
Immediate aciclovir treatment. Oral if appropriate or IV with hospitalisation
Considerindwelling urinary catheter
Analgesia and other supportive methods
Advise risk of recurrence
Advise about possible transmission
541
Q

What are the components of semen?

A

Seminal vesicles release alkaline fluid containing prostaglandins, clotting factors and fructose. This makes up roughly 60% of ejaculate
Prostate releases milky, slightly acidic fluid containing citric acid, proteolytic enzymes and acid phosphatase. This makes up about 25% of ejaculate
Bulbourethral glands release alkaline fluid containing mucus for lubrication but this only makes a tiny contribution to ejaculate volume

542
Q

Roughly how much sperm and semen is ejaculated each time?

A

Around 2-4 ml of semen containing 20-200x10^6 sperm per ml each time

543
Q

Roughly what proportion of sperm swim forward (correct motility)?

A

Normally over 60%

544
Q

Roughly what proportion of sperm will have abnormal morphology?

A

Less than 30%

545
Q

What is ‘emission’?

A

The movement of ejaculate into the prostatic urethra with secretions from accessory glands, by peristalsis of vas deferens

546
Q

What are some female physiological changes that aid coitus?

A

Swelling and engorgement of external genitalia
Vaginal lubrication
Internal enlargement of vagina
If just oestrogen present, forms an abundant, clear non-viscous mucus at the cervix
If oestrogen and progesterone are present, forms a thick, sticky mucus plug

547
Q

Describe the process of ejaculation

A

Contraction of glandular and ductal smooth muscle
Contraction of internal sphincter of bladder
Rhythmic contraction of stratal muscle (ischiocavernosus, bulbospongiosus, anal muscles, hip muscles, pelvic floor)

548
Q

What drives the process of ejaculation?

A

Is a spinal and cerebral reflex arc, driven by L1-L2

549
Q

Describe the changes undergone by sperm in transport to fallopian tubes

A

At ejaculation, sperm is coagulated by seminal vesicle secretions. Most sperm is lost through tha vagina and doesn’t proceed to the cervix. Sperm is reliquefied around 15 minutes after ejaculation and travels through cervix and uterus, where it undergoes capacitation and acrosomal reaction and then up through fallopian tubes

550
Q

What drives capacitation and acrosomal reaction of sperm?

A

Risking cAMP and Ca2+ levels

551
Q

What drives the transport of sperm?

A

Propulsive capacity of sperm

Currents formed by motion of ciliated cells

552
Q

What is the process behind the formation of an erection?

A

Tactile and psychogenic stimulants activate autonomic pelvic nerve and somatic pudendal nerve. These stimulate haemodynamic changes such as activation of parasympathetic system, inhibition of sympathetic vasoconstriction and stimulation of NANC nerves that supply arteries, to release NO.
Postganglionic fibres also release ACh which act of endothelial M3 receptors, increasing intracellular Ca2+ and stimulation NO release.
NO enters vascular smooth muscle cells and through GMP GPCR, there’s vasodilation.
There’s straightening of helicine arteries of corpora cavernosa so cavernous spaces are dilated. Bulbospongiousus and ischiocavernosus also compress venous return from corpora cavernosa so corpora become engorged and so there’s an erection

553
Q

How does viagra work?

A

Inhibits the breakdown of cGMP, important in regulation of engorgement of blood vessels and so helps to maintain erection

554
Q

What happens in capacitation?

A

Sperm undergoes maturation.
Loses glycoprotein coat to allow fusion with the cell surface of oocyte
Movement of sperm tail moves from beat like action to whip like
Sperm becomes receptive to oocyte signals

555
Q

What is an acrosome?

A

Anterior portion of head of the sperm

556
Q

What happens in the acrosomal reaction?

A

Sperm comes into contact with the zona pellucida and their membranes fuse. Acrosome then swells and releases its contents by exocytosis and then there’s penetration of the zona pellucida

557
Q

What are the processes behind fertilisation of an ovum?

A

At ovulation, a secondary oocyte is released, is picked up by fimbriae which directs occyte towards the ampulla. The capacitated sperm loses its acrosome so that it can penetrate the oocyte membrane and fuse with it, forming a zygote. Zygote undergoes meiosis to become diploid and undergoes mitosis and metabolic changes until cleavage occurs and a morula is formed. Eventually a blastocyst is formed that will enter uterine cavity and implant

558
Q

What are the processes behing polycystic ovarian syndrome?

A

Inappropriate feedback from ovary to HPG axis. There’s lack of pulsatile GnRH release and many follicles are developing but none are selected and there’s inappropriate oestrogen secretion.
Abnormal oestrogen leads to increased insulin resistance and risk of endometrial malignancy

559
Q

What are some natural methods of contraception?

A

Abstinence
Coitus interruptus
Rhythm method

560
Q

Using the rhythm method, over what days is fertility assumed?

A

If regular 28 day cycles, days 7-16

561
Q

What contraception methods prevent sperm from entering ejaculate

A

Vasectomy

562
Q

What contraception methods prevent ovulation?

A

Combined Oral Contraceptive Pill
Depot progesterone injection
(progesterone only pill and progesterone implant)

563
Q

What contraception methods prevent transport along fallopian tube?

A

Sterilsation - occludes fallopian tubes using clips, rings or ligation

564
Q

What contraception methods prevent sperm passing through cervix?

A

Progesterone only pill and implant

565
Q

What contraception methods prevent sperm reaching the cervix?

A

Condoms
Diaphragm
Cervical cap
Spermicide

566
Q

What contraception methods prevent implantation?

A

Hormonal contraception
Post coital contraception
Intrauterine device

567
Q

How does the intrauterine device work?

A

Inert/copper that contains progesterone.
Copper interferes with endometrial enzymes and can interfere with sperm transport to fallopian tubes
Can aso be post-coital contraception up to 5 days after ovulation

568
Q

What is infertility?

A

The failure to conceive within one year. Can be primary (no previous pregnancies) or seconday

569
Q

How is infertility managed?

A

Investigate history of STIs/ regular unprotected intercourse, ovulation patterns, tube patency, sperm count
Treat with ovulation inducement, surgery or IVF to overcome occlusion, artficial insemination or intracytoplasmic sperm injection to overcome sperm problems

570
Q

What are some causes of infertility?

A

Coital problems
Anovulation
Tubal occlusion
Abnormal/absent sperm production

571
Q

What are some causes of anovulation?

A

Physiological
Hyperprolatinaemia, weight loss, exercise or stress affecting pulsatile GnRH release
Pituitary tumours or necrosis inhibiting LH/FSH release
Ovarian failure, menopause , chemotherapy or radiotherapy affecting ovarian release of oestrogen and progesterone

572
Q

What is the normal range of the menstrual cycle?

A

21-35 days

573
Q

How can evidence of ovulation be gained?

A

21 day progesterone

Daily waking temperature recordings as progesterone elevates basal temperature

574
Q

What drug can be used to treat hyperprolactinaemia?

A

Bromocriptine (dopamine agonist)

575
Q

How can patency of uterine tubes be investigated?

A

Hysterosalpingography - passage of radioopaque dye through tubes from uterine cavity

576
Q

How can disturbed cervical transport of sperm be investigated?

A

Taking post-coital test of cervical mucus

577
Q

Why is FSH selectively inhibited in PCOS?

A

Follicles release inhibin which inhibits FSH release but not LH release

578
Q

Why is there no LH surge in PCOS?

A

High levels of androgens and androgens inhibit LF surges

579
Q

What happens to the different foetal cavities as pregnancy progresses?

A

Yolk sac disappears with umbilicus as remnant
Amnion grows
Chorion regresses due to amniotic growth

580
Q

How does the conceptus implant into the uterus?

A

Determined by invasive nature of trophoblast cells. Uterine epithelium is breached and conceptus implants into stroma via trophoblast cells.

581
Q

What is meant by the fact that placental membrane is haemomonochorial?

A

Only one layer of trophoblast cells separates the maternal and foetal circulation

582
Q

How do placental villi change over time?

A

Intially, (end of week 2) villi are simply fingerlike projections of trophoblast cells with syncytiotrophoblasts surrounding cytotrophoblast
A few days later, mesenchyme cells start to infiltrate into the core of the villi
Roughly day 23, Foetal vessels invade into the mesenchyme core

583
Q

What are the aims of implantation?

A

Establish basic unit of exchange by placental cilli
Anchor the placenta
Establish maternal blood flow within the placenta

584
Q

What is the decidual reaction?

A

Changes undergone by endometrial epithelium on implantation. Stroma swells and becomes oedematous, occurring due to higher levels of glycogen and other nutrients. Increased secretory function of the endometrium around the site of implantation

585
Q

What are decidual cells?

A

Endometrial cells that have undergone decidual reaction. Have upper stratum compactum, the stratum spongiosum and then stratum basalis, with which the trophoblast cells communicate

586
Q

How does the endometrium prepare for pregnancy after implantation?

A

Decidualisation

Remodelling of spiral arteries to provide low resistance vascular bed to increase blood flow

587
Q

What are the differences between placenta in first trimester and at term?

A

At first trimester, barrier is still relatively thick but this thins as foetal needs increase. Also, a complete layer of cytotrophoblast underlies the syncytiotrophoblast. However, at term, most of this has coalesced to form more syncytiotrophoblast cells. At term there’s also a much increased surface area available for exchange

588
Q

How does foetal blood flow interact with maternal blood flow?

A

Two umbilical arteries take deoxygenated blood from foetus to placenta to exchange with maternal circulation. One umbilical vein takes oxygenated blood from the placenta to the foetus. Villi contain foetal vessels and separate cotyledones receive blood from maternal spiral arteries. These are at high pressure and so force blood deep into the intervillous spaces where they can bath the villi in oxygenated blood

589
Q

Where do intervillous spaces lie?

A

Between the chorionic and decidual plates and in between and surrounding villi

590
Q

Where do villi develop in relation to decidua?

A

Only remain at point of decidua basalis, not where there’s only decidua parietalis

591
Q

How do cotyledons form?

A

Speta form in decidua that project into the intervillous spaces but don’t reach the chorionic plate. This occurs in month 4/5. These have a core made of maternal tissue but are covered in complete layer of syncytiotrophoblast so maternal circulation is always separated from foetal

592
Q

What substances are transported across the placenta?

A

Water, electrolytes, urea and uric acid, and gases travel by simple diffusion
Glucose moves across by facilitated diffusion
Amino acids, iron and vitamins are actively transported.

593
Q

What teratogenic and other damaging substances and organisms can be transported across the placenta?

A

Alcohol, thalidomide and therapeutic drugs are teratogenic.
Also, maternal smoking, drugs of abuse, varicella zoster, triponema pallidum, rubells, cytomegalovirus and toxoplasma gondii can travel across and cause damage

594
Q

What can rubella in pregancy cause in the foetus?

A

Cataracts
Patent ductus arteriosus
Microcephaly

595
Q

What are the metabolic functions of the placenta?

A

Synthesises glycogen, fatty acids and cholesterol

596
Q

What are the endocrine functions of the placenta?

A

Produces steroid hormones (oestrogen and progesterone) As well as protein hormones such as hCG, hCS etc

597
Q

What is the function of human chorionic gonadotrophin?

A

Pregnancy specific protein hormone produced by the placenta that maintains the corpus luteum and is produced in the first 2 months of pregnancy

598
Q

In what pathological conditions can human chorionic gonadotrophin be produced?

A

In males, in some testicular tumours

In females, in premalignant hydatidiform mole or in malignant choriocarcinoma

599
Q

What is the function of human chorionic somatotomotrophin?

A

Influences maternal metabolism to make foetus priority, especially in relation to glucose.

600
Q

What are the different degrees of monozygotic twinning that can occur?

A

1 zygote that splits into two morulas so there are two amnions and two chorions.
1 morula that splits and has 2 bilaminar disks. There are two amnions but foetuses share a chorion
I bilaminar disk from which 2 primitive streaks develop. Share both an amnion and a chorion

601
Q

How is haemolytic disease of the newborn treated prophylactically?

A

If rhesus groups of mother and child are incompatible, mother is given rhesus specific IgG antibodies. This means that on exposure to foetal rhesus, the IgG given will react before the mother’s immune system

602
Q

What changes occur in the cardiovascular system during pregnancy?

A

Increased blood volume so increased caridac output, increased stroke volume and increased heart rate
Decreased systemic vascular resistance due to progesterone action on smooth muscle
Reduced blood pressure in first two trimesters due to compression of central arteries by uterus
Upward displacement of the heart
Cardiac hypertrophy
Flow murmurs common
Venous distension

603
Q

What changes occur in the urinary system during pregnancy?

A

Increased glomerular filtration rate and therefore increased functional renal reserve
Increased renal plasma flow
Reduced levels of urea, uric acid, bicarbonate and creatinine (increased filtration)
Increased RAAS activation

604
Q

What are some complications that can occur in urinary system durng pregnancy?

A

Progesterone causes smooth muscle relaxation of ureters that can lead to ureteric stasis, hydroureter, increased risk of UTI and increased risk of pyelonephritis

605
Q

Why is pyelonephritis in pregnancy worrying?

A

Gives increased risk of pre-term labour

606
Q

What changes occur in the respiraory system during pregnancy?

A

Displacement of diaphragm
Widening of intercostal angle
Increased AP and transverse diameter of the thorax
Reduced functional residual capacity (unchanged vital capacity so total capacity changes little)
Increased alveolar ventilation rate
Increased tida volume.
Physiological hyperventilation due to progesterone increasing respiratory drive coupled with increased CO2 production from metabolism.

607
Q

What buffers respiratory alkalosis produced by physiological hyperventilation in pregnancy?

A

Increased excretion of bicarbonate at the kidneys

608
Q

What changes occur in carbohydrate metabolism during pregnancy?

A

Increased peripheral insulin resistance so body uses gluconeogenesis and other methods. Maternal metabolism altered to prioritise foetal glucose needs so there is reduced fasting blood glucose and raised post-prandial glucose

609
Q

What hormones promote insulin resistance in pregnancy?

A
Oestrogen
Progesterone
Prolactin
Human placental lactogen
Cortisol
610
Q

How is lipid metabolism altered in pregnancy?

A

In first trimester, progesterone stimulates appetite and the deposition of maternal fat. In second trimester there is stimulation of lipolysis to increase plasma levels of free fatty acids, to be used as a substrate for maternal metabolism in the absence of intracellular glucose

611
Q

What changes occur to thyroid hormones in pregnancy?

A

Increased production of thyroid binding globulin and increased T3 and T4, however free T4 is in normal range. hCG also directly stimulates production of T3 and T4 at the thyroid so they exert negative feedback, lowering TSH levels

612
Q

What changes occur in the gastrontestinal system during pregnancy?

A

Alteration of deposition of abdominal viscera due to enlargement of uterus
Progesterone stimulated smooth muscle relaxation leads to delayed GI emptying, stasis of biliary tract and an increased risk of pancreatitis

613
Q

What haematological changes occur in pregnancy?

A

Pregnancy is a prothrombotic state due to increased fibrin deposition at implantation site, increased fibrinogen and other clotting factors, reduced fibrionolysis, venodilation and stasis of blood

614
Q

How does immune system adapt in pregnancy?

A

Foetus is an allograft so there’s non-specific suppression of the immune system and the materno-foetal interface.
Also, IgG antibodies can transfer but not antibodies for rhesus/ABO except for in secondary haemorrhage in rhesus incompatability

615
Q

Why is there physiological anaemia in pregnancy?

A

Increased plasma volume with associated increase in red cell mass but not equivalent to plasma increase. This means that there’s a relative anaemia

616
Q

What are some risks of gestational diabetes?

A
Macrosomic foetus
Prematurity
Impaired lung maturation
Respiratory disorders of newborn 
Risk of congenital defects
Polycythaemia
617
Q

What are some risk factors for gestational diabetes?

A

BMI >30
Past history of gestational diabetes or macrosomic foetus
Family history of diabetes
South asian/carribbean ethnicity

618
Q

What are some signs and symptoms of pre-eclampsia?

A
Hypertension
Proteinuria
Peripheral oedema
Pulmonary oedema
Headaches
Vision changes
Vomiting
Thought disturbances
Slow foetal growth 
Albuminuria
Oliguria
Thrombocytopenia
Oligohydramnios
619
Q

What is the placental barrier made up of during the first trimester?

A

Syncytiotrophoblast
Cytotrophoblast
Connective tissue
Foetal capillaries

620
Q

What is the placental barrier made up in the third trimester?

A

Syncytiotrophoblast

Foetal capillary endothelium

621
Q

How does alcohol cross the placental membrane?

A

By simple diffusion as it’s lipid soluble

622
Q

What is shed from the uterus post-partum?

A

Placenta and decidua

623
Q

How does early pregnancy support itself?

A

Through secretion of hCG from the developing conceptus. hCG stimulates and maintains progesterone and oestrogen levels that come from the corpus luteum. The oestrgoen and progesterone can then maintains the endometriuma and so support the pregnancy

624
Q

What is the benefit of hCG suppressing maternal humeral immunity?

A

Means that maternal immune system won’t attack placenta and vice versa

625
Q

Why is oestriol a useful indicator of foetal progress?

A

Levels depend on the foetal adrenals, liver and placenta

626
Q

What are some consequences of venous distension in pregnancy?

A

Can get haemorrhoids and varicose veins

627
Q

How does placenta help to promote foetal skeletal growth?

A

Placenta produces calcitriol which is an active form of vitamin D. This therefore increases the uptake of calcium from the maternal gut, increasing the availability to the foetus

628
Q

What are some potential risks of gestational diabetes after labour?

A

In utero, will have been foetal hyperglycaemia so foetal insulin will have been stimulated and glucose is stored as fat.
Birth is difficult due to large foetal size.
After birth, there’s a reflex foetal hypoglycaemia due to the high levels of circulating insulin the the blood. Hypoglycaemia can quickly damage the brain due to its lack of glycogen levels

629
Q

How is physiological anaemia of pregnancy treated?

A

Oral iron sulphate, or gluconate

630
Q

What effect does smking in pregnancy have?

A

Shifts maternal bohr shift to the left due to CO levels, there’s then reduced oxygen levels available for the foetus. Will then be growth retardation - low birth weight

631
Q

What is eclampsia?

A

Seizures in pregnancy

632
Q

How are eclamptic fits managed?

A

Maintaining maternal airway, giving oxygen and putting mother on her left side to enhance uterine perfusion
Magnesium given to stop systemic vasospasm and so stop fit
Control blood pressure
Assess foetus
Deliver foetus

633
Q

Why is hyperreflexia important to assess in pre-eclampsia?

A

Sign of the effect of worsening vasospasms on the CNS so can indicate progression to eclampsia

634
Q

What can the result of poor foetal nutrition in late pregnancy be?

A

Asymmetrical growth restriction and oligohydramnios

635
Q

What can the result of poor foetal nutrition in early pregnancy be?

A

Neural crest defects

636
Q

How does foetak circulation change on its first breath?

A

Hypoxic pulmonary vasoconstriction reduces and so there’s reduced resistance in pulmonary vessels, increasing venous return to left atrium until pressure in left atrium is greater than in the right so foramen ovale closes.
Increased pO2 coupled with no more prostaglandins coming from placenta constricts the ductus arteriosus so blood no longer passes from pulmonary arteries to aorta. Stasis in the umbilical vein and the ductus venosus leads to clots forming in these vessels and subsequent fibrosis so this shunt also closes

637
Q

What isthe function of the foetal kidney?

A

Functional foetal kidney is the metanephros which produces hypotonic urine which foetus constantly swallows

638
Q

How much urine is produced by the foetus?

A

At week 25, produces around 100ml urine per day and at term, produces around 500ml

639
Q

What happens to amniotic fluid when it’s swallowed by the foetus?

A

Foetus absorbs the water and electrolytes which will all be filtered again at the metanephros. Any debris from the fluid, however, accumulates in the foetal gut and will eventually be expelled as the meconium (first foetal poo)

640
Q

What problems can be indicated by too early or failure to pass the meconium?

A

If it’s passed prematurely, is a sign of foetal distress and can cause respiratory problems in the child if aspirated. If it’s not passed soon after birth, is a sign of cystic fibrosis causing meconium ileus

641
Q

How is amniotic fluid formed?

A

In early pregnancy, formed by maternal fluids as well as diffusion of foetal extracellular fluid across the nonkeratinised skin of the foetus.
Later in the pregnancy however, is produced and removed by the foetus itself

642
Q

Why can the amniotic fluid be diagnositically useful?

A

Contains cells from the amnion as well as cells from the foetus itself so can give insight into any problems with the foetus

643
Q

How is bilirubin dealt with by the foetus?

A

Can’t conjugate it itself so it accumulates and is then transferred to the mother to deal with. This needs to change quickly after birth of jaundice can result

644
Q

How can bilirubin conjugation in newborn be stimulated?

A

By phototherapy which makes bilirubi easier to deal with

645
Q

What factors help to maximise oxygen supply to the foetus?

A

Has much lower pO2 of 4kPa maximum so forms a very steep concentration gradient
Has more haemoglobin per dl of blood
Haemoglobin doesn’t have beta chains which means it can’t bind 2,3-DPG so has a much higher affinity for oxygen
Low diffusion resistance

646
Q

How is CO2 transfer optimised between mother and foetus?

A

Concentration gradient needs to be established but can’t make foetus have higher levels of CO2 as it won’t tolerate it.
Instead, progesterone stimulates physiological maternal hyperventilation, lowering maternal pCO2 so CO2 can cross the placenta more easily

647
Q

How is oxygen supply to maximised and prevented from mixing with deoxygenated blood?

A

WHen oxygenated blood enters at the umbilical vein, mixes with deoxygenated blood at the IVC but this only lowers the pO2 slightly. When blood enters the right atrium, it is directed towards the foramen ovale by the crista dividens of septum secundum so blood passes into left atrium, left ventricle, aorta and then arteries to the brain.
Deoxygenated blood from the brain enters SVC, right atrium, right ventricle and then pulmonary artery but is directed to the aorta, distal to the outflow to the brain, through the ductus arteriosus

648
Q

What are the stages of development of the respiratory system?

A

In foetal period, the bronchopulmonary tree forms
From week 8-16 - pseudoglandular stage where ducts form between bronchopulmonary segments. These ducts will go on to form bronchioles
Week 16-24 - canaliculi stage - respiratory bronchioles bud off bronchioles formed in pseudoglandular stage
Week 24 onwards - terminal sac stage - sacs bud off from respiratory bronchioles. Type 1 and type 2 pneumocytes start to differentiate from one another and surfactant is produced

649
Q

In the foetus, what is the threshold for viability?

A

Week 24 onwards as lungs need to have entered the terminal sac stage

650
Q

What is the purpose of the foetuses respiratory movements?

A

Lungs filled with fluid and gas exchange occurs across the placenta so movements are to condition the respiratory musculature

651
Q

What changes occur to the nervous system in the foetal period?

A

Brain is earliest organ to start developing and last to finish.
Corticospinal tracts develop in 4th month for coordinated voluntary movement.
Myelination of nuclei and tracts
Cerebral hemisphere becomes largest part of the brain so gyri and sulci form as brain grows quicker than the skull
Histological differentiation of the cortex
Relative growth of the spinal cord and vertebral column

652
Q

When is the foetal heart fully formed?

A

Around week 15

653
Q

What is the normal foetal heart rate?

A

110-160 bpm. If less than 100, sign of foetal distress

654
Q

When does definitive foetal kidney start to function?

A

Week 10

655
Q

When do foetal sensory and motor systems develop?

A

Movement starts in week 8 and can be detected on ultrasound but isn’t detectable by mother until week 17 - quickening

656
Q

What’s the difference between asymmetrical and symmetrical growth restrictions?

A

Symmetrical is a generalisd and proportional growth restriction. Indicates slow development throughout and has higher risk of permanent neurological sequelae. Can occur in maternal substance abuse or anaemia
Asymettrical growth restriction is where there’s reduced abdominal growth but relative sparing of head growth. Often due to causes later in gestation such as high blood pressure/malnutrition

657
Q

How can foetal age be estimated?

A

Estimate duration of pregnancy by fertilisation age or time since last menstrual perod
Use developmental criteria such as crown rump length, biparietal diamet, abdominal circumference and femur length, weight and appearance after delivery or foot length
Measure symphysis-fundal height

658
Q

How is symphysis fundal height measured?

A

Measure from maternal pubic symphysis to top of fundus with tape measure or assessing fundus in relation to other structures such as umbilicus/xiphisternum

659
Q

What can cause variation in symphysis-fundal height?

A

Number of foetuses
Lie of foetus
Extent of engagement of head
Volume of amniotic fluid

660
Q

What’s the difference between oligohydramnios and polyhydramnios?

A

Oligo-is too little amniotic fluid, probably due to foetal renal impairment or placental insufficiency
Poly-Is too much amniotic fluid, probably due to deformity such as inability to swallow

661
Q

How can foetal daily rhythms be used to assess the foetus?

A

Foetus has daily rhythms of activity, heart rate and respiratory movement. Especially heart rate variations is useful as it indicates development of control systems

662
Q

What systems does assessment of foetal tone look at?

A

MSK and nervous (episodes of flexion/extension)

663
Q

What systems does a non-stress test look at?

A

Looks at heart rate changes in response to movement so CVS and autonomic nervous system

664
Q

What are some factors that can impact on foetal growth?

A
Maternal nutrition and health
Uteroplacental blood flow
Efficiency of placenta
Maternal habits
Maternal parity
Genetic factors
Race
Maternal weight and height
665
Q

Why is week 20 a good point to carry out foetal assessments?

A

At this point organ systems are formed so anomolies can be identified, with enough time to intervene if necessary
Inherent error of measurements increases with time

666
Q

What are alpha-fetoprotein levels used for when monitoring a pregnancy?

A

If high can detect an open neural tube defect or a multiple pregnancy

667
Q

When can foetal heartbeat be heard?

A

With transvaginal ultrasound from week 5/6

With doppler stethoscope from week 10/12 and with normal stethoscope from week 18/20

668
Q

How do foetal respiratory movements change in roughly week 34?

A

Respiratory movments occur is bursts, punctuated by episodes of apnoea and hiccups

669
Q

How can development of foetal liver be assessed?

A

Foetal abdominal circumference.

670
Q

When can a foetus be classifed as at risk?

A
In maternal hypertension
In maternal heart or liver disease
In multiple gestation
In maternal diabetes
If there's evidence of growth retardation
If oligohydramnios is suspected
If there's presence of placental abnormality
In a post-dated pregnancy
671
Q

What are the approximate AP and transverse diameters of the normal gynecoid pelvis?

A

AP - 10.5

transverse - 11

672
Q

What are the features of an anthropoid pelvis?

A

Narrow transverse diameter

Narrow side walls

673
Q

What are the features of an android pelvis?

A

Narrow forepelvis

Narrow sub-pubic arch

674
Q

What are the features of a platypelloid pelvis?

A

Narrow AP diameter

675
Q

What happens to the cervix to make it more amenable to birth?

A

Undergoes ripening, stimulated by progesterone. This reduces amount of collagen fibres but increases amount of glycosaminoglycans in matrix.

676
Q

What are the patterns of contractions at different points in the pregnancy?

A

Early pregnancy - of low amplitude and occur every 30 mins (approx) they are not detectable as pain
Later on, frequency reduces but amplitude increases so they might be detectable as pain and these are know as braxton hicks contractions.
Then, under the action of prostaglandins and oxytocin right at the end of pregnancy, contractions become closer together and more forcefull until there’s brachystasis where fibres don’t relax as much as they contract and this acts to increase the intrauterine pressure

677
Q

Where doe uterine contractions begin?

A

At two lateral poles of uterus, across the fundus and then down the body. This creates a wave to expel the foetus from the upper segment

678
Q

In relation to labour, where are prostaglandins made?

A

In decidua, placenta, myometrium, membranes and endometrium. Controlled by the oestrogen/progesterone ratio

679
Q

What is the ferguson reflex?

A

Refers to positive feedback whereby oxytocin and prostaglandins act to initiate cervical ripening and uterine contractions. These contractions stretch the cervix and vagina and this send afferent messages to the hypothalamus to stimulate further oxytocin release from the posterior pituitary gland. Therefore, there’s further contraction and further stretching etc

680
Q

What is the 1st stage of labour?

A

Between onset and full cervical dilation. Has latent phase where there’s slow dilation of variable rate, up to around 4cm.
Then active phase where dilation occurs at roughly 1-1.2 cm per hour. This phase also involves regular uterine contractions

681
Q

What is the second stage of labour?

A

Woman experiences urge to bear down and presenting part of foetus appears in the birth canal. Baby flexes head, internally rotates, head is delivered, extends head, externally rotates head and then rotates shoulders and is fully delivered.

682
Q

What is the third stage of labour?

A

Expulsion of placenta due to rapid, forceful contractions of the uterus

683
Q

How is blood loss after labour minimised?

A

COntraction of myometrium compresses myometrial blood vessels
Once placenta and membranes have been delivered, contracting uterus applies pressure to its own walls
Torn vessels from shearing off initiates the blood clotting cascade

684
Q

What is meant by the life of a foetus?

A

It’s position in relation to the long axis of the uterus

685
Q

What is meant by the presentation of a foetus?

A

Which part is adjacent to the inlet

686
Q

What are some different cephalic presentations of the foetus?

A

Synciput - head is unflexed
Brow - head is extended
Face - head is fully extended

687
Q

What are the different types of breach presentations of the foetus?

A

Frank breach with legs fully extended upwards
Full breach with legs curled upwards
Single fooling breach - only fot is in contact with the cervix. Will be insuffiecient stretching of the cervix and so will require c-section

688
Q

What is meant by the position of the foetus?

A

The orientation of the presenting part

689
Q

How may labour be induced?

A

Giving prostaglandins and oxytocin

690
Q

Why may labour fail to progress?

A

Insufficient powers
Insufficient passage
Abnormalities of passenger

691
Q

What scoring system is used to assess the condition of the neonate?

A

Apgar score which ranges from 0-10.
0 points are given each if baby is blue, flaccid, impalpable pulse, absent respiration and absent response
1 point is given each for blue baby, rigid, pulse 100bpm, regular respiration and normal response

692
Q

What is colostrum?

A

Type of milk produced by mother in first few days after labour. Has less sugar, fat and water than mature milk but more proteins, specifically immunoglobulins

693
Q

What is the general structure of a non-lactating breast?

A

Made up of glands and supportive tissue, embedded in a fatty matrix, as well as blood vessels, lymphatics and nerves. Mammary glands are embedded in the normal breast tissue. Lobules and ducts combine to form lactiferous ducts closer to the nipple.
Each lobe consists of alveoli, ducts, blood vessels and a lactiferous duct

694
Q

How does structure of the breast change from birth to adulthood?

A

At birth, a few ducts are present.
At puberty, these ducts start to branch and connect with others. There’s also increase in the number of lobules and in the amount of interlobular stroma
During the luteal phase of the menstrual cycle, mammary glands grow further by cell proliferation and can be oedema in stroma. After menstruation, there’s decrease in lobule size
With increasing age, there’s decrease in size and number of terminal duct lobular units and stroma is replaced by adipose tissue

695
Q

What are the anatomical boundaries of the breast?

A

Medial - Lateral sternal edge
Lateral - mid-axillary line
Superior - 2nd rib
Inferior -6th rib

696
Q

How is breast prepared for lactation during pregnancy?

A

High levels of oestrogen and progesterone in pregnancy stimulate the growqth of breast tissue but inhibit secretion from glands. Steroid hormones stimulate ducto-lobular-alveolar hypertrophy and prominent lobules form and alveolar lumens become dilated. There’s reduction in interlobular stroma. Half way through the pregnancy, aleolar cells differentiate so that they can produce milk

697
Q

What are the components of mature milk?

A

90% water from mothers system
7% lactose, synthesised in mammary glands
2% fat made in smooth endoplasmic reticulum in alveolar cells
Proteins made on golgi apparatus as well as immunoglobulins from mother’s system
Mineral and vitamins from mother’s system
Energy value = 27MjperL

698
Q

How is milk production hormonally controlled?

A

After birth and the loss of the placenta, steroid hormone concentrations fall so secretion can be stimulated. There’s also increased sensitivity of alveolar cells to prolactin
Suckling of the newborn then stimulates a neuro-endocrine reflex which stimulates the hypothalamus to stop production of dopamine and so stimulate prolactin production from the anterior pituitary gland. Prolactin then stimulates secretion from alveolar cells

699
Q

What stimulates the ‘let down reflex’?

A

Suckling stimulates a neuroendocrine reflex where oxytocin release is stimulated from the posterior pituitary gland and this acts on myoepithelial cells around the alveolar cells to contract and so let down the milk

700
Q

What structural changes occur in the breast on cessation of lactation?

A

Lobules atrophy but not to their original size

701
Q

What are accessory nipples?

A

Milk line remnants of polythelia and accessory breast tissue that can occur at any point along the milk line

702
Q

What are some benign epithelial lesions?

A

Fibrocystic change
Epithelial hyperplasia
Papilloma

703
Q

What is fibrocystic change?

A

Most common breast lesion. There’s cyst formation, fibrosis and apocrine metaplasia of breast tissue. Often presents as a mammographic abnormality or a mass that disappears on fine needle aspiration

704
Q

What is epithelial hyperplasia in the breast?

A

Proliferation of epithelia that fills and distends ducts giving a slightly incresed risk of carcinoma, especially if cells are atypical

705
Q

How is epithelial hyperplasia of the breast found?

A

As incidental finding on biopsy

Mammographic abnormality

706
Q

What is a papilloma?

A

Benign intraduct lesion with multiple fibrvascular cores that are covered in epithelium and myoepithelium
Presents as nipple discharge, palpable mass or a mammographic abnormality

707
Q

Where in the breast do papillomas occur?

A

Large papillomas tend to occur singularly at lactiferous ducts.
Smaller papillomas can be multiple and tend to lie deeper in the breast with an increased risk of carcinoma

708
Q

What are some inflammatory conditions that can affect the breast?

A

Acute mastitis
Duct ectasia
Fat necrosis

709
Q

What causes acute mastitis?

A

Normally a staph aureus infection that gets through cracks and fissures in the nipple and almost always occurs with lactation

710
Q

What are some symptoms of acute mastitis?

A

Painful, erythematous breast
Pyrexia
Breast abscess

711
Q

How is acute mastitis treated?

A

Antibiotics and encourage milk expression

712
Q

What is duct ectasia?

A

Dilatation and inflammation of mammary gland ducts resulting in periarealor mass and bloody or serous dnipple discahrge.
Often in women in their 50/60s

713
Q

How does fat necrosis of the breast normally present?

A

As a mass, skin changes or calcification on mammography. Often with a history of trauma or surgery

714
Q

What are some stromal tumours of the breast that can occur?

A

Fibroadenoma
Phylloes tumour
Gynaecomastia

715
Q

What is a fibroadenoma?

A

A mass that’s usually highly mobile and can grow very large and take over the whole breast. Can be uni-or bilateral. Forms a well defined, greyish, rubbery mass that’s made up of a mixture of stroma and epithelia

716
Q

What is a phyllodes tumour?

A

A mass that can grow very large and take over the whole breast. Presents as a mass or mammographic abnormality and forms nodules of proliferating stroma that is often atypical and highly cellular, that’s covered in epithelium. Can be benign, borderline or malignant and macroscopically is reddish/brown and clefted and may bleed.
Requires excision with a large margin or it can recur

717
Q

How do malignant phyllode’s tumours behave?

A

Aggressively and spread through the blood stream to metastasise. Can recur locally.

718
Q

What is gynaecomastia?

A

Benign enlargement of the male breast that can be uni-or bilateral, often in puberty or in old age.

719
Q

What causes gynaecomastia?

A

Relative decrease in androgens or increase in oestrogen so occur in
puberty,
in neonates due to circulating oestrogens
Klinefelter’s syndrome
Oestrogen excess,eg in cirrhosis
In gonadotrophin excess, eg in functional testicular tumours
Or can be drug related

720
Q

What are some common presentations of brest disease?

A
Pain
Palpable mass
Nipple discharge
Mammographic abnormality
Skin changes
721
Q

What are some differentials for pain in the breast?

A

If cyclical and diffuse then is likely to be physiological

If non-cyclical and focal, could be ruptured cyst, due to injury or inflammation, or could be malignancy

722
Q

What are some differentials for palpable mass in the breast?

A

May be normal nodularity

If hard, craggy and fixed, may be invasive carcinoma, fibroadenoma or a cyst

723
Q

What are some differentials for nipple discharge?

A

If milky - endocrine disorder or side effect of medication
If bloody or serous - duct ectasia, papilloma or malignancy
In general, if discharge is spontaneous and unilateral, is more worrying

724
Q

What do mammographies try and detect?

A

Density
Calcification
Parenchymal deformity

725
Q

What are some differentials for a density on mammography?

A

Invasive carcinoma
Fibroadenoma
Cyst

726
Q

What are some differentials for calcification on mammography?

A

Ductal carcinoma in situ

Benign changes

727
Q

How is breast disease investigated and diagnosed?

A

Clinically through history, family history and examination
Do mammography or ultrasound imaging
Take fine needle aspiration cytology
Core biopsy

728
Q

What are some risk factors for the development of breast cancer?

A
Gender
Uninterrupted menses
Early menarche (<11)
Late menopause
Breast feeding
Obesity/high fat diet
Exogenous oestrogens
Reproductive history
Geographic influence
Radiation exposure
Previous mammographic/biopsy abnormalities
Previous breast cancer
Hereditary
729
Q

What is an in situ carcinoma of the breast?

A

One that has neoplastic population of cells that is limited to the ducts and lobules by the basement membrane. This means that the myoepithelium is preserved and as it can’t invade into blood vessels, won’t metastasise

730
Q

What is ductal carcinoma in situ?

A

In situ carcinoma of cells sitting within ducts showing central necrosis and calcification. Mostly pre-invasive but can progress to invasive after a number of years.
Can spread extensively through ducts and lobules without crossing the basement membrane

731
Q

What is paget’s disease of the breast?

A

Extension of ductal carcinoma in situ whereby the cancerous cells grow up towards the skin of the nipple but sill without crossing the basement membrane. Produces a red, crusting nipple that can be confused with eczematous or inflammatory condition

732
Q

What is an invasive carcinoma of the breast?

A

Carcinoma that invades beyond the basement membrane into the stroma and so can invade into vessels and metastasise.
Can present as a mass or mammographic abnormality but by the time it’s palpable, most cases will have already spread to axillary lymph nodes

733
Q

What is invasive ductal carcinoma - no special type?

A

Invasive carcinoma of the breast that accounts for majority of breast cancers.
Can be well differentiated with tubules lined by atypical cells
Or can be poorly differentiated where there are sheets of pleomorphic cells

734
Q

What is invasive lobule carcinoma?

A

Invasive carcinoma of the breast that tends to present more as a thickening of breast tissue, rather than a lump so may present later than invasive ductal.
Cells are infiltrative and appear in single file with lack of cohesion.
Can occur bilaterally

735
Q

How does p’eau d’orange of the skin of the breast occur?

A

If lymphatic drainage of the breast is affected in invasive carcinoma. There is then lymphoedema of the breast tissue but fixed hair follicles appear indented in comparison

736
Q

What is the general pattern of metastasis of breast cancer?

A

Can spread in lymphatics to ipsilateral lymph node

Can spread in blood to bone, lung, liver or brain

737
Q

Where are some unusual sites that certein type of breast cancer can spread to?

A

Invasive lobular carcinoma can spread to peritoneum, retroperitoneum, ovaries, GI tract, uterus and leptomeninges

738
Q

What does the prognosis of breast cancer depend on?

A
If it's in situ or invasive
Histological subtype
Stage
Grade
Gene expression profile
739
Q

How can breast cancer be treated through local and regional control?

A

Breast surgery - may be mastectomy or breast conserving
Axillary surgery
Post operative radiotherapy

740
Q

What does the extent of breast surgery in breast cancer depend on?

A
Patient's wishes
Site of tumour (central/peripheral)
Size of tumour
Relative size of breast
Type of cells involves
741
Q

What are the different types of axillary surgery that can be done in breast cancer?

A

Extent depends on nodes involved.
Can carry out sentinel sampling, whereby the first draining lymph nodes of the breast are identified through radiological marking. This means that only the first few nodes can be removed and this reduces effect of lymphoema and subsequent malignancy risk
Can also carry out axillary dissection if widespread

742
Q

What effect does the molecular classification of a breast cancer have on treatment?

A

If oestrogen receptor positive (brown staining nuclei) then can treat with tamoxifen
If HER2 receptor positive, can treat with herceptin (brown staining membrane)

743
Q

How can breast cancer be systemically controlled?

A

Chemotherapy if appropriate
Hormonal treatment
Herceptin

744
Q

How can survival from breast cancer be increased?

A

Early detection, through increasing awareness, knowledge of family history, self examination and regular mammographic screening
Neoadjuvant therapy (chemo before surgery if metastatic)
Use of newer therapies
Use of gene expression profiles
Prevention in familial cases through genetic screening and maybe prophylactic mastectomies

745
Q

What is the precursor of vulval cancer and how does it present?

A

Vulval intraepithelial neoplasia (grades 1-3)
Presents as:
Scaly red patches
Sore itchy vulva
White plaques
Can occur around labia, perineum and perianal
Often found incidentally

746
Q

What are the main types of vulval carcinoma?

A

Squamous
Basal Cell
(adenocarcinoma, malignant melonoma)

747
Q

What are he risk factors for vulval cancer?

A

In young women, HPV 16+18 (same as cervical)

In older women, cronic irritation, eg from squamous hyperplasia and other skin conditions)

748
Q

What is the histology of VIN?

A

Abnormal maturation
Mitotic activity and basaloid cells above the basal layer
May be keratotic

749
Q

What is paget’s disease of the vulva?

A

Squamous carcinoma that spread down into tissues and so has an association with invasive carcinoma. This is very difficult to excise

750
Q

Where does squmous carcinoma normally form and how does it appear?

A

Normally at labia but can be anywhere. Forms a keratotic, wart or ulcerated lesion

751
Q

How does basal cell carcinoma of the vulva usually present?

A

As a pearly white or pigmented nodule that’s often ulcerated and mainly at the labium majora. This can be deeply infiltrative but doesn’t metastasise and so doesn’t require a vulvectomy

752
Q

How dovulval tumours spread?

A

Can spread to anus, urethra, vagina.

Spreads to inguinal lymph nodes and femoral artery. At this point, becomes very problematic and is usually fatal

753
Q

How does vulval cancer present, in general?

A

A lump or ulceration with itching and irritation
May be local bleeding and discharge
May be dysuria and dyspareunia

754
Q

What are the main precursors of cervical cancer?

A

Cervical intraepithelial neoplasia is precursor to squamous carcinoma
Cervical Glandular intraepithelial neoplasia is precursor to adenocarcinoma

755
Q

How is Cervical Intraepithelial Neoplasia graded?

A

1-3
Based on mitotic activity,
pleomorphism,
nuclear to cytoplasm ratio

756
Q

What is the histology of CIN3?

A

Abnormal surface cells
Mitotic activity above the basal layer
Basaloid cells limited to basal layer still

757
Q

How does squamous carcinoma of the cervix present?

A

Post coital, intermenstrual or post-menopausal bleeding

Maybe dyspareunia

758
Q

What is the histological appearance of cervical squamous carcinoma?

A

Expansion of the cervix with nodules/ulceration

Infiltrating tongues of squmous carcinoma form as well as usual cytological hallmarks of malignancy

759
Q

What are the risk factors for cervical cancer?

A
Multiple sexual partners
Early first sexual partner
Cigarette smoking
Familial disposition
Long term use of OCP
Immunosuppression
Early first pregnancy
Multiple pregnancies
760
Q

How can cervical cancer spread?

A

Locally around cervix to uterus then around the uterus to bladder and rectum
Can spread in lymphatics to paracervical, paraaortic and pelvic lymph nodes

761
Q

What are the two types of endometrial adenocarcinoma?

A

Type 1 mostly due to unopposed oestrogne

Type 2 - more sinister. Clear cell and uterine serous papillary tumou. Mostly in post-menopausal women

762
Q

What is an endometrial adenocarcinoma?

A

Malignancy of glandular epithelium

763
Q

What does the prognosis of endometrial adenocarcinoma depend on?

A

Depth
Grade/type
Involvement of cervical stroma or adnexa
Associated hyperplasia

764
Q

Where does endometrial adenocarcinoma spread to?

A

To myometrium, cervix and adnexa

765
Q

What is endometrial carcinosarcoma?

A

A malignancy of endometrial glands and their stroma that can also contain heterologous elements such as bone

766
Q

What is endometrial stromal sarcoma?

A

Malignancy of glandular supportive tissue so looks like stroma but has round or elongated spindle cells

767
Q

What is leiomyoma?

A

Benign growth of myometrial smooth muscle that’s oestrogen dependent, presenting as heavy and painful periods and mass symptoms

768
Q

How does leiomyoma appear on histology?

A

Interlacing bundles of smooth muscle cells

769
Q

What is leiomyosarcoma?

A

Malignancy of myometrial smooth muscle cells with features of malignancy, producing swelling, abdominal discomfort, pain and bleeding

770
Q

How does leiomyosarcoma metastasis?

A

In blood to the lungs

771
Q

What are the different types of endometrial hyperplasia?

A

Simple- cystic glands with abundant stroma
Complex - branching, budding or crowded glands
Complex with atypia - cytological features of malignancy