Repro Flashcards

1
Q

Define haemomonochorial

A

There is only one layer of trophoblast separating the maternal blood from the fetal capillary wall

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2
Q

What are the aims of implantation?

A

Establish basic unit of exchange

  • primary villi = trophoblast
  • secondary = mesenchyme invasion
  • tertiary = invasion of fetal vessels

Anchor the placenta

Establish maternal blood flow in the placenta

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3
Q

What features prepare the endometrium for implantation?

A

The presence of pre-decidual cells

Spiral artery elaboration and remodelling - creating a cytotrophoblast lining

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4
Q

Explain the importance of decidualisation

A

This provides the balancing force to the invasive force of the trophoblast. Limits the depth of implantation

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5
Q

Which layers of the embryo go on to form the placenta?

A

Synctiotrophoblast

Cytotrophoblast

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6
Q

Why is there increased invasion during an ectopic pregnancy?

A

There are no decidual cells to limit the extent of implantation.

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7
Q

Why are the spiral arteries remodelled?

A

to create a low resistance vascular bed

to maintain the high flow required to meet fetal demands

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8
Q

What causes pre-eclampsia?

A

inadequate remodelling of the spiral arteries. There is no cytotrophoblast lining.

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9
Q

What is the reason for placental insufficiency?

A

invasion is incomplete

blood vessels are not deep enough

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10
Q

How does the placenta change between the first trimester and full term?

A

First trimester - complete cytotrophoblast layer beneath the synctiotrophoblast
full term - cytotrophoblast layer is lost, thinning the placental barrier. Surface area increased.

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11
Q

Give two examples of an infectious agent that can cause developmental defects in the placenta

A

Varicella zoster
cytomegalovirus
toxoplasmosa gondii
rubella

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12
Q

Describe the arrangement of fetal blood vessels within the placenta

A

the two umbilical arteries, bringing deoxygenated blood from the fetus to the placenta, spread out along the chorionic plate, giving off a main stem villus at points. these then ive branch villi. Exchange with maternal blood occurs in the intervillous space.
there is one umbilical vein bringing oxygenated blood from the placenta to the fetus.
SEE DIAGRAM.

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13
Q

Why is compression of the umbilical cord so dangerous?

A

Gas exchange is flow limited, not diffusion limited
Compression leads to decreased flow, leading to compromised gas exchange.
Fetal oxygen stores are small, so adequate flow is essential

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14
Q

Which substances have specific receptors on the synctiotrophoblast to be actively transported across the placenta?

A

aas
iron
vitamins

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15
Q

What metabolic substrates are synthesised by the placenta?

A

glycogen
cholesterol - used to make steroid hormones
fatty acids

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16
Q

What protein based and steroid hormones are produced by the placenta?

A

Protein

  • hCG
  • human chorionic somatomammotrophin
  • human chorionic thyrotrophin
  • human chorionic corticotrophin

steroid

  • progesterone
  • oestrogen
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17
Q

What is the function of the steroid hormones produced by the placenta?

A

They maintain the pregnant state

progesterone increases appetite

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18
Q

At what week does the placenta take over the role of producing progesterone and oestrogen from the corpus luteum?

A

week 11

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19
Q

What is the function of hCS?

A

increase glucose availability to the fetus

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20
Q

What is a molar pregnancy?

What result does this give on pregnancy testing?

A

= no fetal tissue, just an outer cell mass

Gives +ve result as hCG is produced by the placenta

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21
Q

How is passive immunity via the placenta achieved?

A

Receptors on the synctiotrophoblast for IgG antibodies.

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22
Q

What is the cause of haemolytic disease of the new born?

A

Rhesus incompatibility between the mother and the fetus leads to the mother creating IgG against different rhesus group. These can cross the placenta in a future pregnancy and cause immune destruction of the fetal RBCs.
prophylactic treatment is now given to prevent the immune response in the first pregnancy of the mother

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23
Q

What is the function of hCG?
Where is it produced?
For how long?

A

supports secretory function of corpus luteum
synctiotrophoblast
first two months of pregnancy

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24
Q

How does the cardiovascular system change in pregnancy?

A

Blood volume increases to compensate for blood loss at birth
therefore cardiac output, stroke volume and heart rate increase
resistance decreases in order to maintain a low or normal blood pressure

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25
Q

How does progesterone affect the blood vessels in pregnancy?

A

Relaxes smooth muscle

Decreases TPR

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26
Q

How does the position of the gravid uterus affect blood return to the heart?

A
aortocaval compression 
decreases return of blood to heart
decreases pre load
decreases stroke volume
decreases blood pressure
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27
Q

How does pregnancy affect the urinary system?

A

increase in renal plasma flow
increase in GFR
decrease in functional renal reserve as there is limited capacity for compensation

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28
Q

How is the respiratory system changed in pregnancy?

A
the diaphragm is displaced and the AP and transverse diameters of the thorax increase
Leading to...
decreased functional residual capacity
increased tidal volume
increased ventilation
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29
Q

Describe the physiological hyperventilation in pregnancy

A

there is increased CO2 production
progesterone increases the respiratory drive by acting at the respiratory centres in the brain
this leads to respiratory alkalosis

this is compensated by increased renal bicarbonate excretion

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30
Q

How is a mother’s metabolism changed in pregnancy?

A

Human placental lactogen (as well as prolactin, cortisol and oestrogen/progesterone) increases maternal peripheral insulin resistance.
Metabolism switches to gluconeogenesis and alternative fuels
Lipolysis increases in T2, leaving glucose for the fetus to use

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31
Q

How does pregnancy affect thyroid function?

A

increase in Thyroid binding globulin production
therefore increase in T3/T4

hCG decreases TSH production, so it’s levels stay within normal range

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32
Q

What are the effects of progesterone on the GI system?

A

smooth muscle relaxes
delayed emptying
stasis in the biliary tract leading to gall stones and pancreatitis

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33
Q

How does pregnancy affect blood coagulation?

A

Pregnancy is a pro-thrombotic state
increased fibrinogen and clotting factors
reduced fibrinolysis
therefore PE etc can occur

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34
Q

How is the fetus not rejected by the immune system in pregnancy?

A

there is non-specific suppression of the local immune response at the materno-fetal interface.

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35
Q

What causes pre-eclampsia?

A

Defect in placentation, leading to poor uteroplacental circulation.
Systemic endothelial dysfunction leads to vasoconstriction of blood vessels and the plasma contraction.

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36
Q

Why does urinary stasis occur in pregnancy?

A

Progesterone relaxes smooth muscle
ureters become obstructed
Can cause UTI.
Pyelonephritis increases the risk of preterm labour

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37
Q

Define gestational diabetes

A

carbohydrate intolerance first recognised in pregnancy and not persisting after delivery

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38
Q

Why are mothers with gestational diabetes considered high risk pregnancies?

A

Macrosomic fetus
stillbirth
congenital defects

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39
Q

Describe the clinical features of pre-eclampsia

A
new hypertension
new proteinuria
headache
swelling of hands, face and feet
liver tenderness
visual disturbance
fetal distress - reduced movements
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40
Q

What is HELLP syndrome?

A

Haemolysis, Elevated Liver enzymes, Low Platelets

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41
Q

What are the symptoms of gestational anaemia?

A

Fatigue
dyspnoea
dizziness
pallor

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42
Q

which blood vessel connects the hypothalamus to the anterior pituitary gland?

A

Superior hypophyseal artery

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43
Q

Which hormones bind to the mammotrophic cells in the anterior pituitary gland?

Where are they produced?

A

Prolactin releasing hormone and prolactin inhibiting hormone

Hypothalamus

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44
Q

Where does prolactin act?

A

Mammary glands

Testes

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45
Q

In males, which hormone does FSH stimulate the release of?

From what cells?

A

Inhibin

Sertoli cells

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46
Q

In males, which hormone does LH stimulate the release of?

From what cells

A

Testosterone

Leydig cells

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47
Q

In females, which cells does FSH act on?

What hormone do these cells release?

A

Granulosa cells

Inhibin

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48
Q

In females, what cells does LH act on?

Which hormone/s do these cells secrete?

A

Theca cells

Oestrogen and progesterone

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49
Q

What are the two stages of the ovarian cycle?

A

Follicular

Luteal

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50
Q

What are the uterine stages of the menstrual cycle?

A

Menses
Proliferative
Secretory

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51
Q

Variation in cycle length is because of variation In which ovarian phase?

A

Follicular phase

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52
Q

What is the length of the literal phase of the menstrual cycle?

A

14 days

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53
Q

Name the five parts of the Fallopian tube

A
Fimbria 
Infundibulum 
Ampulla
Isthmus
Intramural part
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54
Q

Describe the layers of the wall of the Fallopian tube

A

Inner mucosa - folded. Columnar. Some are Ciliated. Peg cells secrete mucus.
Muscular layer (x2 in ampulla, x3 in isthmus)
Serosa

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55
Q

Describe the two layers of the endometrium

A

Stratum functionalis - this is shed. Coiled arteries

Stratum basalis. Straight arteries.

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56
Q

Which hormones dominate in the stages of the endometrial cycle?

A

Proliferative phase - oestrogen

Secretory phase - progesterone

Menstrual - drop in progesterone

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57
Q

How do falling levels of progesterone lead to menstruation?

A

Spiral arteries in the stratum functionalis spasm
It is deprived of nutrients
Necrosis

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58
Q

What are the boundaries of the cervix?

A

Internal os

External os

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59
Q

Describe the epithelium of the cervix

A

Simple columnar epithelium
Changes to non-keratinised stratified squamous on the inner aspect of the external os
Mucus secreting glands

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60
Q

Describe epithelium of the vagina

A

Non-keratinised stratified squamous

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61
Q

How does oestrogen influence the vaginal epithelium?

A

Causes them to accumulate glycogen
This is a substrate for lactobacillus
Leads to acidic pH

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62
Q

How is the vagina lubricated?

A

It has no glands of its own

The cervical glands and vestibular glands secrete mucus

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63
Q

What percentage volume of semen is produced by the seminal vesicles?

A

60%

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64
Q

What is the fluid produced by the seminal vesicles composed of?

A

alkaline fluid
fructose
prostaglandins
clotting factors - fibroinogen, holds sperm in place after ejaculation

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65
Q

What percentage volume of semen is produced by the prostate gland?

A

25%

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66
Q

What is the fluid produced by the prostate gland composed of?

A

milky slightly acidic fluid
proteolytic enzymes - breakdown clotting factors, causing liquefaction of sperm
citric acid
phosphotase

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67
Q

What is the fluid produced by the bulbourethral glands composed of?

A

alkaline fluid

mucous - lubricates the end of the penis and urethral lining

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68
Q

What are the phases of the sexual response cycle?

A

excitement
plateau
orgasm
resolution

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69
Q

Describe the excitement phase of the male sexual response

A

limbic system activated
sacral parasympathetic neurons are activated
thoracolumbar sympathetic neurons are inhibited
ACh to M3 leads to increased [Ca2+]. NO synthase activated
NO leads to vasodilation in the corpora cavernosa
penis fills (latency) and undergoes tumescence (erection)

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70
Q

Describe the plateau phase of the male sexual response

A

activation of sacrospinous reflex
contraction of ischiocavernosus so crus of penis is compressed.
venous return impeded. venous engorgement
accessory glands stimulated to secrete fluid and lubricate distal urethra and neutralise acidic urine

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71
Q

Describe the orgasmic phase of the male sexual response

A

Emission
thoracolumbar spinous reflex activated
smooth muscle of vas deferens, ampulla, seminal vesicle and prostate contract
internal and external urethral sphincters contract
semen pools in urethral bulb

Ejaculation
under cortical control
sympathetic nervous system (L1-2) activated
contraction of smooth muscle of glands, ducts and urethral sphincter
filling of urethra stimulates the pudendal nerve
genital organs, ischiocavernosus and bulbocavernosus muscles contract
semen is expelled

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72
Q

Describe the resolution phase of the male sexual response

A

thoracolumbar sympthtic pathway activated
arteriolar smooth muscle in corpora cavernosa contracts
causes increased venous return
detumescence
refractory period

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73
Q

Describe the excitement phase of the female sexual response

A

limbic system activated
sacral parasympathetic neurons are activated
thoracolumbar sympathetic neurons are inhibited
ACh to M3 leads to increased [Ca2+]. NO synthase activated
NO leads to vasodilation in the clitoris
vaginal lubrication begins
uterus elevates
increase in muscle tone, heart rate and blood pressure

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74
Q

Describe the plateau phase of the female sexual response

A

further increase in muscle tone, heart rate and blood pressure
labia minora deepen in colour
clitoris withdraws under its hood
bartholin glands secrete fluid to lubricate the vestibule
formation of orgasmic platform in lower 1/3rd of vagina
full elevation of uterus

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75
Q

Describe the orgasmic phase of the female sexual response

A

the orgasmic platform contracts rhythmically 3-15 times
uterus and anal sphincter contract
no refractory period, so multiple orgasms are possible

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76
Q

Describe the resolution phase of the female sexual response

A

clitoris descends and engorgement subsides
labia return to unaroused size
uterus descends
vagina shortens and narrows

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77
Q

What are some reasons for erectile dysfunction?

A
  • Psychological (descending inhibition of spinal reflexes)
  • Tears in fibrous tissue of corpora cavernosa
  • Vascular: atherosclerosis, diabetes
  • Drugs: Alcohol, anti-hypertensives (β-blockers, diuretics)
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78
Q

What is the mechanism of action of Viagra?

A

inhibits cGMP breakdown

more NO

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79
Q

What are the effects of high oestrogen levels on cervical mucus?

A

abundant mucus
clear
non-viscous

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80
Q

What are the effects of high progesterone levels on cervical mucus?

A

thick, sticky mucus plug

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81
Q

What changes to the sexual occur with ageing in females?

A

reduced desire
reduced vasocongestion response, causing reduced vaginal lubrication
vaginal and urethral tissues lose their elasticity and the length and width of the vagina decrease and hence there is reduced expansible ability of inner vagina during arousal. The number of orgasmic contractions is often reduced and a more rapid resolution occurs.

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82
Q

describe the transport of sperm through the cervix and uterus

A

clotting factors lead to coagulation of semen - prevents sperm falling out of vagina
reliquefaction of sperm occurs 20 minutes later
most sperm leak out of the vagina
transport into the uterus is by their own propulsive capacity
the ciliated cells in the uterine tract help
oxytocin stimulates uterine contraction

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83
Q

What is capacitation?

A

maturation of sperm in the female reproductive tract

removal of the glycoprotein coat - allows fusion with the oocyte cell surface

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84
Q

What is the acrosomal reaction?

A

sperm binding to the ZP3 of the zona pellucida triggers the acrosome reaction
exocytosis of the contents of the acrosome

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85
Q

What induces capacitation and the acrosomal reaction?

A

influx of calcium

rise in cAMP

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86
Q

Describe the regions of the oocyte plasma membrane

A

smooth surface directly overlying the metaphase chromosome

Microvilli cover the rest. Sperm bind and fuse here.

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87
Q

Define syngamy

A

male and female pronuclei unite to form one diploid gamete

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88
Q

What is the fast block reaction?

A

wave of depolarisation starting at site of entry of sperm into the oocyte
prevents polyspermy

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89
Q

Define polyploidy

A

embryo contains three or more pronuclei

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90
Q

What is the fertilw window of the menstrual cycle?

A

days 7-16

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91
Q

How long can sperm survive in the female?

A

maximum of 7 days

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92
Q

how long does the oocyte survive after ovulation?

A

1 day

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93
Q

How is a vasectomy performed?

A

vas deferens is divided bilaterally

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94
Q

How does progesterone act as a contraceptive?

A

creates thick cervical mucus plug, preventing sperm from entering uterus
thins uterus lining making implantation less likely
negative feedback at the hypothalamus decreases GnRH, so follicular development is inhibited

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95
Q

How does the combined oestrogen and progesterone pill act as a contraceptive?

A

negative feedback at hypothalamus and anterior pituitary inhibits follicular development
loss of positive feedback mid-cycle, so no LH surge

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96
Q

How does the intrauterine device act as a contraceptive?

A

copper interferes with endometrial enzymes

interferes with implantation

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97
Q

How does post-coital contraception work?

A

high dose of oestrogen and progesterone/progesterone only up to 72 hours after coitus
disrupts ovulation
blocks implantation
impairs luteal function

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98
Q

Define infertility

A

failure to conceive within one year

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99
Q

What is the difference between primary and secondary infertility?

A
primary = no previous pregnancy
secondary = previous pregnancy, successful or not
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100
Q

What are some reasons for male infertility?

A

abnormal sperm production
duct obstruction
hypothalamic/pituitary dysfunction

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101
Q

Describe the pathophysiology polycystic ovarian syndrome

A

Increased gonadotrophin-releasing hormone (GnRH) pulsatility or high levels of insulin caused by insulin resistance.
leads to excess LH produced by the anterior pituitary
ovaries are stimulated to produce excessive amounts of male hormones, particularly testosterone.

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102
Q

What are the symptoms of polycystic ovarian syndrome?

A
Oligomenorrhoea (defined as light or infrequent menstrual periods)
Infertility or subfertility
Acne
Hirsutism - excessive hair growth
Alopecia
Obesity or difficulty losing weight
Psychological symptoms - mood swings, depression, anxiety, poor self-esteem
Sleep apnoea
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103
Q

Define parturition

A

transition from the pregnant state to the non-pregnant state

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104
Q

What are the terms used to describe labour depending on the week of birth

A

Before 24 weeks = spontaneous abortion
Before 36 weeks = pre-term
Between 37 and 42 weeks = term
After 42 weeks = post-term.

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105
Q

What happens in the first stage of labour?

A

creation of the birth canal
full cervical dilation
regular uterine contractions

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106
Q

What happens in the second stage of labour?

A

expulsion of the fetus
rapid
bear down and push
presenting part of the fetus appears in the birth canal

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107
Q

What name is given to the parts of the fetus as it presents?
head
buttocks, shoulder or knee
foot

A

head = crowning
buttocks, shoulder or knee = breech
foot = footling breech

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108
Q

Describe the movement of the fetus in the second stage of labour if the head is presenting

A
head flexes as it reaches pelvic floor (reducing presentation diameter)
head internally rotates
head stretches the vagina and perineum
head delivers
shoulders rotate and deliver
rest of baby follows!
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109
Q

What happens in the third stage of labour?

A

effect of uterine contractions increased as the fetus has been expelled
contraction of the uterus and expulsion of the placenta

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110
Q

How is haemorrhage reduced in the third stage of labour?

How can this effect be enhanced?

A

uterus contracts down hard
blood vessels compressed, closing them off

oxytocic drug

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111
Q

What determines the size of the birth canal?

A

bony pelvis

surrounding ligaments - soften to increase size

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112
Q

What is cervical ripening?

A

the softening of the cervix

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113
Q

How does cervical ripening occur?

A

cervix is made of tough, thick, coiled collagen
The actions of Prostaglandins PG E2 and F2x cause:
• Reduction in collagen production (Turnover altered)
• Increase in glycosaminoglycans (Disrupts the matrix)
• Increase in hyaluronic acid (draws water in)
• Reduces aggregation of collagen fibres (Uncoils)

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114
Q

What does effacement of the cervix describe?

A

the thinning and flattening of the cervix

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115
Q

What forces the cervix apart?

A

contractions of the uterus

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116
Q

What is the diameter of a fully dilated cervix?

A

10cm

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117
Q

What are ‘Braxton-Hicks’ contractions?

A

practice contractions

irregular in intensity and timing

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118
Q

Uterine contractions occur throughout pregnancy.

What prevents labour occurring?

A

progesterone supresses the contractions

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119
Q

What makes the contractions of the uterus more forceful and frequent?

A

prostaglandins

oxytocin

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120
Q

How do prostaglandins make the contractions of the uterus more forceful?

A

increase the [Ca2+] per action potential

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121
Q

How does oxytocin make the contractions of the uterus more frequent?

A

lowers the threshold, increasing the frequency of contractions

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122
Q

How is the production of prostaglandins controlled?

A

the oestrogen : progesterone ratio
If Progesterone > Oestrogen (as in most of pregnancy), there will be low levels of prostaglandins

If Oestrogen > Progesterone (as at the end of pregnancy)
Leads to increased Prostaglandin levels
This means that the cervix is ripened and uterine contractions are promoted

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123
Q

Where are prostaglandins produced?

A

endometrium

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124
Q

Where is oxytocin produced?

A

posterior pituitary

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125
Q

How is oxytocin release stimulated

A

Ferguson Reflex
prostaglandins cause contraction of the myometrium
positive feedback to hypothalamus
more oxytocin released from the posterior pituitary
stimulates increased contractions and more prostaglandin release

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126
Q

What induces oxytocin receptors to appear on the uterus?

A

oestrogen

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127
Q

Define brachystasis

What is the consequence of this in the uterus?

A

uterine muscle relaxes less than it contracts
fibres shorten in the body of the uterus
forces the presenting part of the fetus into the cervix

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128
Q

What does the Ferguson Reflex cause?

A

the more the cervix stretches, the more oxytocin is released

the more the uterus contracts!

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129
Q

What causes the fetus to take its first breath?

A

trauma
cold
light
noise

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130
Q

What causes the ductus venosus to close?

A

the clamping of the umbilical cord

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131
Q

What causes the foramen ovale to close?

A

fetus takes first breath, decreases tissue resistance in the lungs as they expand
decreases vascular resistance in lungs
blood flows into lungs
drop in P on right side of heart
higher P in left atrium forces foramen ovale to close

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132
Q

What causes the ductus arteriosus to close?

A

decrease in P in right atrium results in reversal of flow through ductus arteriosus (aorta to pulmonary)
increased pO2 causes muscle wall to contract

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133
Q

What is the most common presentation of a fetus?

A

longitudinal
cephalic
well flexed
vertex presents to pelvic inlet

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134
Q

Why might failure of progression in labour occur?

A
inadequate power
inadequate passage
- abnormal bony pelvis
- rigid perineum
abnormalities of the passenger
- too big
- breech
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135
Q

How can labour be induced?

A

prostaglandins

oxytocic drugs

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136
Q

How is a caesarean section carried out?

A

suprapubic incision
linea alba and rectus sheaths resected superiorly
incision through uterus
removal of baby

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137
Q

Define primary postpartum haemorrhage

A

loss of blood estimated to be >500 ml, from the genital tract, within 24 hours of delivery

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138
Q

What does the intermediate mesoderm give rise to?

A

embryonic kidney

gonad

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139
Q

What embryonic cells is the gonad derived from?

A

intermediate mesoderm

primordial germ cells

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140
Q

Where do primordial germ cells arise from?

Where do they migrate to?

A

yolk sac wall

migrate to retroperitoneum along the dorsal mesentery

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141
Q

What do the primordial germ cells develop into?

A

testes

ovaries

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142
Q

Which gene on the Y chromosome drives the development of the male reproductive system?

A

SRY

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143
Q

What is another name for the mesonephric duct?

A

Wolffian duct

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144
Q

What is another name for the paramesonephric duct?

A

Mullerian duct

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145
Q

How is the urogenital sinus created?

A

the urorectal septum divides the hindgut

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146
Q

Where do the paramesonephric ducts appear?

A

on the epithelium of the urogenital ridge
as invaginations of epithelium
open into the abdominal cavity and make contact with cloaca

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147
Q

Why does the mesopnephric duct disappear in females?

A

no androgen secretion

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148
Q

Which gender secretes Mullerian Inhibiting Substance in development?

A

males

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149
Q

What does Mullerian Inhibiting Substance cause?

A

the paramesonephric duct to degenerate

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150
Q

What stimulates the external male genitalia to form?

A

dihydrotestosterone

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151
Q

What does the paramesonephric duct go on to form?

A

uterine tubes, uterus and upper portion of vagina

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152
Q

What stimulates the external female genitalia to form?

A

oestrogen

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153
Q

Describe the descent of the testes

A

testes begin in peritoneum
testes descend close to processus vaginalis, pulled by the gubernaculum
end in scrotum with tunica vaginalis surrounding

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154
Q

Describe the descent of the ovary

A

gubernaculum attaches inferiorly to labio-scotal folds
ovary descends into pelvis
round ligament of the uterus lies in the inguinal canal

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155
Q

Describe the external genitalia at 7 weeks

A

identical!
genital tubercle anteriorly
urogenital sinus with surrounding genital folds and genital swelling

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156
Q

Describe how the male external genitalia are formed between weeks 7 and 12

A

androgens
genital tubercle elongates
genital folds fuse to form spongy urethra

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157
Q

Describe how the female external genitalia are formed between weeks 7 and 12

A

there is no fusion of the genital folds

urethra opens into vestibule

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158
Q

How does duplication of the uterus occur?

A

lack of fusion of the paramesonephric ducts

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159
Q

What is hypospadias?

A

incomplete fusion of urthral folds on inferior surface of penis
abnormal openings into the urethra

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160
Q

Why does micropenis occur?

A

insufficient androgen stimulation

primary hypogonadism or hypothalamic/pituitary dysfunction

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161
Q

Describe the pathogenesis of Congenital Adrenal Hyperplasia

A
21-hydroxylase deficiency
cortisol cannot be made
low cortisol means high ACTH
constant stimulation leads to hyperplasia of adenal gland
high amount of androgens
male-like features in females
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162
Q

Describe the pathogenesis of Androgen Insensitivity Syndrome

A
XY genotype with testes
lack of androgen receptors
tissues fail to respond to androgens
male genitalia are not stimulated to develop
sexual ambiguity
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163
Q

Where are spermatozoa produced?

A

seminiferous tubules

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164
Q

Describe the route from the seminiferous tubules to the epididymis

A
seminiferous tubules
straight tubule
rete testis
efferent ductule
epididymis
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165
Q

Name the three parts of the epididymis.

Which is most proximal?

A

head - most proximal
body
tail

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166
Q

What are the two coverings of the testes?

A

tunica vaginalis - peritoneum

tunica albuginea - fibrous

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167
Q

Where is the tunica vaginalis derived from?

A

peritoneum

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168
Q

What surfaces of the testicles does the tunica vaginalis cover?

A

anterior surface

sides

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169
Q

Where is the tunica vasculosa found?

A

between the tunica albuginea and the seminiferous tubules

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170
Q

Where is perilobar tissue found?

What is found in this tissue?

A

between seminiferous tubules

Leydig cells - secrete testosterone

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171
Q

In the seminiferous tubules, what cells are found?

A

Lateral - spermatogonia
spermatocytes
medial - spermatids

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172
Q

Where are Sertoli cells found?

A

in the seminiferous tubule epithelium
extend from basement membrane to lumen
connected by tight junctions - creating the blood testis barrier

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173
Q

What is the function of the Sertoli cells?

A

support of the germ cells
provide nutrients
phagocytose excess spermatid cytoplasm

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174
Q

What is spermatogenesis?

Where does this process occur?

A

mitosis of spermatogonia to form primary spermatocyte
meiosis of primary spermatocytes to form 4 spermatids

seminiferous tubules

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175
Q

What is spermiogenesis?

A

spermatids develop into spermatozoa

rete testis, efferent ducts, completed in epididymis

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176
Q

How are spermatids transported from the seminiferous tubules to the epididymis?

A

peristaltic contractions

sertoli cell secretions

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177
Q

Define the spermatogenic cycle

What is the length of this?

A

time taken for the reappearance of the same stage of spermatogenesis within the same segment of the tubule

16 days

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178
Q

Define the spermatogenic wave

A

distance between the same stage of spermatogenesis within the tubule

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179
Q

What is the function of the rete testis?

A

fluid reabsorption

sperm concentration

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180
Q

What is the function of the epididymis?

A

head stores sperm until it is ready to undergo maturation

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181
Q

What is the function of the vas deferens?

A

transports mature sperm to the ejaculatory duct

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182
Q

Where does the ejaculatory duct form?

A

union of the vas deferens and the duct of seminal vesicle

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183
Q

Describe the epithelium of the rete testis

A

columnar ciliated cells - for movement of sperm

cuboidal non-ciliated cells - for absorption

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184
Q

Describe the epithelium of the epididymis

A

pseudostratified columnar with stereocilia

smooth muscle on outside layer

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185
Q

Describe the epithelium of the vas deferens

A

folded pseudostratified columnar epithelium
lamina propria
three layers of smooth muscle - longitudinal, circular, longitudinal

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186
Q

Describe the epithelium of the seminal vesicle

A

highly folded pseudostratified columnar

glandular elements surrounded by muscular coat - sympathetic stimulation

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187
Q

Describe the epithelium of the prostate gland

A
mucosal glands - inner
submucosal glands
main glands - outer
all drain separately into the urethra
fibromuscular capsule separates into lobules
epithelium is heterogenous
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188
Q

In old age, what are commonly seen in histology of the prostate gland?

A

prostatic concretions

lamellated bodies - proteins, nucleic acids, cholesterol and calcium phosphate

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189
Q

Why does the breast enlarge at puberty?

A

oestrogens
accumulation of adipose tissue
lactiferous ducts enlarge

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190
Q

Describe the histology of the lactiferous ducts of the breast

A

lined by cuboidal to columnar epithelium
changes to stratified squamous at level of the lactiferous sinuses
ducts surrounded by myoepithelial cells

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191
Q

How are the breasts changed in the menstrual cycle?

A

oestrogen peak induces duct proliferation
enlargement
oedema
tenderness

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192
Q

When does maximal development of the breast occur?

A

during pregnancy

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193
Q

How is the breast changed in pregnancy?

A

oestrogen results in hypertrophy of the ductular-lobular-alveolar system
progesterone influences alveolar cells differentiation from squamous to columnar cells in order to be capable of milk production from mid gestation

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194
Q

Describe the anatomical location of the female breast

A

extends from lateral border of sternum to the mid-axillary line
overlies the second to sixth ribs.
within the skin overlying the muscles of the anterior thoracic wall.
nipple overlies the fifth intercostal space
circular body and axillary tail

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195
Q

How are the lobules of the breast separated?

A

suspensory ligaments = fibrous connective tissue septa extend from skin to deep fascia

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196
Q

What forms the tubercles of the breast?

A

underlying areolar glands

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197
Q

Where is the retromammary space?

A

between the breast and fascia overlying the chest wall muscles

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198
Q

Describe the blood supply of the breast

A

internal thoracic artery,
intercostal artery and from the lateral thoracic and thoracoacromial arteries.

axillary vein, the posterior intercostal veins and the internal thoracic vein

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199
Q

Describe the lymphatic drainage of the breast

A

lateral quadrants of the breast drain to the axillary lymph nodes.
The medial quadrants drain to the parasternal nodes or the opposite breast

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200
Q

What is a mammary gland?

A

lobulated masses of tissue

made up of lobules of alveoli, blood vessels and Lactiferous ducts

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201
Q

How is milk synthesised in the breast?

A

alveolar cells of the mammary glands
Fats - SER
Protein - Golgi Apparatus
Sugar - Synthesised and secreted

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202
Q

What are the four physiological stages of lactation?

A
  • Mammogenesis = preparation of the breast
  • Lactogenesis = synthesis and secretion from the breast alveoli
  • Galactogenesis = ejection of milk
  • Galactopoiesis = maintenance of lactation
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203
Q

What is colostrum?

A

milk produced in the first week after birth

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204
Q

How is colostrum different to the mature milk produced by the breast?

A

contains less:
water soluble vitamins
fat
sugar

much more:
protein
fat soluble vitamins
immunoglobulins

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205
Q

Describe the composition of mature milk produced by the breast?

A
Water – 90%
Lactose – 7% (Galactose and Glucose disaccharide)
Fat – 2% 
Proteins found in mature milk:
•	Lactoglobulin (maternal IgG)
•	Lactalbumin
Minerals
Vitamins
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206
Q

At birth, what hormonal change leads to milk production?

A

birth -> progesterone and oestrogen levels fall

breast becomes more responsive to prolactin

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207
Q

How is the release of prolactin controlled?

A

release from anterior pituitary under control of hypothalamus

suckling of the breast -> release of prolactin stimulating hormone from hypothalamus = stimulation

dopamine = inhibition

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208
Q

What kind of hormone is prolactin?

A

polypeptide

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209
Q

Where is prolactin released from?

A

anterior pituitary

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210
Q

How is milk let down hormonally controlled?

A

suckling -> oxytocin released from posterior pituitary

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211
Q

How does oxytocin cause milk ejection?

A

causes the myoepithelial cells surrounding the alveoli to contract

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212
Q

What does maintenance of milk production depend on?

A

regular suckling, to promote prolactin secretion to produce milk and oxytocin secretion to remove milk

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213
Q

What are the effects of prolactin in the breast?

A

milk secretion

milk production for next feed

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214
Q

What causes cessation of lactation?

A

no suckling

lower prolactin levels
turgor-induced damage of breast

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215
Q

How does the breast change in old age?

A

Terminal duct lobular units (TDLUs) decrease in number and size
Interlobular stroma replaced by adipose tissue

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216
Q

Which age group are fibroadenomas of the breast most common in?

A
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217
Q

Which age group are Phyllodes tumours of the breast most common in?

A

6th decade

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218
Q

Which age group is breast cancer most common in?

A

> 50 years

rare before 25

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219
Q

How are breast lesions discovered and investigated?

A

Clinical - History, family history, examination
Radiographic Imaging - Mammogram and ultrasound scan
Pathology - Fine needle aspiration cytology (FNAC) and core biopsy

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220
Q

What causes acute mastitis?

A

usually Staph aureus entering nipple cracks during lactation

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221
Q

How does acute mastitis present?

A

Erythematous painful swollen breast

fever

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222
Q

How is acute mastitis treated?

A

expressing milk

antibiotics

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223
Q

What is a complication of acute mastitis?

A

breast abscess

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224
Q

What is duct ectasia?

A

dilation and inflammation of lactiferous duct

can mimic carcinoma clinically

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225
Q

Which age group is duct ectasia most common in?

A

50’s and 60’s

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226
Q

How does fat necrosis of the breast present?

A

mass
skin changes
ill-defined and irregular, spiculated mass-like area on mammogram

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227
Q

What is gynaecomastia?

A

Enlargement of the male breast

Seen at puberty and in the elderly

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228
Q

What is the cause of gynaecomastia?

A

relative androgen decrease and increase in oestrogen

Can indicate hormonal abnormality, cirrhosis of the liver (oestrogen not metabolised effectively) or functioning testicular tumour

Can occur with drugs – Alcohol, marijuana, heroin, anabolic steroids

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229
Q

What are the features of a fibrocystic lesion of the breast?

A

Benign Epithelial Lesion
presents as a mass or mammographic abnormality
Mass often disappears after fine needle aspiration (FNA)
Can mimic carcinoma clinically and mammographically

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230
Q

What does a fibrocystic lesion of the breast look like histologically?

A

Cyst formation,
fibrosis
apocrine metaplasia

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231
Q

What does a papilloma of the breast look like histologically?

A

Intraduct lesion

multiple branching fibrovascular cores covered by myoepithelial and epithelial cells

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232
Q

How does a fibroadenoma of the breast present?

A

a mass, usually mobile

mammographic abnormality

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233
Q

How does a fibroadenoma of the breast appear macroscopically?

A

Well defined boundaries
rubbery
greyish/white

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234
Q

How does a fibroadenoma of the breast appear histologically?

A

a stromal tumour

mixture of stromal and epithelial elements

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235
Q

What is a Phyllodes tumour?

A

stromal breast tumour

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236
Q

How does a Phyllodes tumour of the breast appear histologically?

A

Nodules of proliferating stroma covered by epithelium (phullon = leaf).
Stroma is more cellular and atypical than in fibroadenomas.

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237
Q

What is a complication of a Phyllodes tumour?

A

breast cancer

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238
Q

How is a Phyllodes tumour treated?

A

excised with a wide margin to prevent recurrence

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239
Q

What are the risk factors for breast cancer?

A

Female gender
Long interval between menarche and menopause
Number of children
Age at first full term pregnancy (greater age = more risk)
Not breast feeding
No interruption of oestrogen levels
Obesity and high fat diet
Exogenous oestrogens – HRT slightly increases risk, OCP does not appear to affect risk
Radiation
Genetics

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240
Q

Which genes are associated with an increased risk of breast cancer?

A

BRCA1 or BRCA2 tumour suppressor genes - 3% of all breast cancers and 25% of familial cancers attributed to mutations in these. Lifetime risk for female carriers is 60 – 85%
Median age at diagnosis ~20 years earlier than sporadic cases

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241
Q

What is the reasoning behind most of the risk factors of breast cancer?

A

prolonged oestrogen exposure

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242
Q

What type of cancer are most breast cancers?

A

adenocarcinomas

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243
Q

What is an in situ carcinoma of the breast?

A

Neoplastic population of cells limited to ducts and lobules by basement membrane
Myoepithelial cells are preserved
Does not invade into vessels and therefore cannot metastasise

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244
Q

What causes Paget’s disease of the breast?

A

in situ carcinoma of the breasr extends to the skin of the nipple without crossing the basement membrane

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245
Q

What are the signs and symptoms of Paget’s disease of the breast?

A
Itching.
Erythema.
Scale formation.
Erosions.
Nipple discharge including bleeding
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246
Q

How does a ductal carcinoma in situ present?

A

as mammographic calcifications - Clusters or linear and branching
mass

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247
Q

How does a ductal carcinoma in situ appear histologically?

A

central necrosis with calcification

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248
Q

What is an invasive carcinoma in the breast?

A

Carcinoma invaded beyond the basement membrane into the stroma
Can invade vessels and therefore can metastasise to lymph nodes and other sites

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249
Q

How does an invasive carcinoma present?

A

mass
mammographic abnormality
peau d’orange - impaired lymphatic drainage

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250
Q

Where does breast cancer metastasise to?

A

Lungs
bones
liver
brain

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251
Q

How does an invasive lobular carcinoma appear histologically?

A

Infiltrating cells in a single file

cells lack cohesion

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252
Q

Where does an invasive lobular carcinoma metastasise to?

A
peritoneum
retroperitoneum
leptomeninges
gastrointestinal tract
ovaries
uterus
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253
Q

What is sentinel lymph node sampling?

What is the benefit of this?

A

Intraoperative lymphatic mapping with dye/radioactivity to find the first draining lymph node - most likely to contain breast cancer metastases

If sentinel node is negative, axillary dissection can be avoided

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254
Q

What is the mechanism of action of tamoxifen?

A

nonsteroidal agent that binds to oestrogen receptors (ER), inducing a conformational change in the receptor.
results in blockage or change in the expression of oestrogen dependent genes
prevents stimulation of growth of tumour

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255
Q

What is the mechanism of action of Herceptin?

A

used in Her2 (human epidermal growth factor receptor) positive cancers
monoclonal antibody binding to HER2 receptors
inhibits proliferation of cells
flags cells for destruction by immune system

256
Q

How can survival rates of breast cancer be improved?

A
Early detection
- Awareness of disease, importance of family history, self-examination, mammographic screening
Neo-adjuvant chemotherapy
- Early treatment of metastatic disease
Gene expression profiles
Prevention in familial cases
 - Genetic screening
 - Prophylactic mastectomies
257
Q

What organism is genital herpes caused by?

A

Herpes simplex virus types 1 and 2

258
Q

What organism is chlamydia caused by?

A

Chlamydia trachomatis

259
Q

What organism is gonorrhoea caused by?

A

Neisseria gonorrhoeae

260
Q

What organism is syphilis caused by?

A

Treponema pallidum

261
Q

What organism is trichomoniasis caused by?

A

Trichomonas vaginalis

262
Q

What kind of organism is Chlamydia trachomatis?

A

gram -ve
intracellular
cocci

263
Q

What kind of epithelium does Chlamydia trachomatis infect?

A

columnar

transitional

264
Q

What are the complications of a chlamydia infection?

A

Women:
PID
ectopic pregnancy
tubal infertility

Men:
epididymitis
epididymo-orchitis

265
Q

Describe the chlamydia screening programme

A

Offers testing to all previously or currently sexually active patients (male and female) aged 25 years or under opportunistically
Testing should be repeated annually or after a change in sexual partner.
Testing for men = first-void urine sample and,
for women = a self-taken vaginal swab or urine sample

266
Q

Describe the clinical presentation of chlamydia in males

A

ASYMPTOMATIC in 50%
urethritis with dysuria and urethral discharge
epididymo-orchitis presenting as unilateral testicular pain ± swelling.
Fever
Epididymal tenderness.
Perineal fullness due to prostatitis

267
Q

Describe the clinical presentation of chlamydia in females

A

ASYMPTOMATIC in 80%
Mucopurulent endocervical discharge.
Dysuria (always consider chlamydia as a cause of sterile pyuria).
Vague lower abdominal pain and abdominal tenderness.
Fever.
Intermenstrual or postcoital bleeding.
Dyspareunia = painful sexual intercourse
A friable, inflamed cervix, sometimes with a follicular or ‘cobblestone’ appearance, with contact bleeding.
Pelvic adnexal tenderness on bimanual palpation.

268
Q

What are some of the systemic features of a chlamydia infection?

A
  • Reactive arthritis, common in young adults. Reiter’s syndrome is a
  • Upper abdominal pain due to perihepatitis (Fitz-Hugh and Curtis syndrome) is a presenting feature.
  • Proctitis with mucopurulent discharge which may be due to rectal chlamydia following anal intercourse.
  • Pharyngeal infection (although this is uncommon and usually asymptomatic with chlamydia).
269
Q

What is Reiter’s Syndrome?

A

triad of urethritis, arthritis and conjunctivitis that can be triggered by chlamydial infection (amongst other pathogens), usually in conjunction with HLA-B27.

270
Q

What is the treatment for chlamydia?

A

doxycycline

azithromycin - single dose

271
Q

What kind of organism is Neisseria gonorrhoeae?

A

gram -ve
intracellular
diplococcus

272
Q

Describe the clinical presentation of gonorrhoea in males

A
  • urethral infection - Mucopurulent or purulent discharge and/or dysuria
  • Rectal infection - usually asymptomatic; may cause anal discharge or perianal/anal pain, pruritus or bleeding
  • Pharyngeal infection - usually asymptomatic
  • Epididymal tenderness/swelling or balanitis (rare)
273
Q

Describe the clinical presentation of gonorrhoea in females

A
  • Endocervical infection - frequently asymptomatic, increased or altered mucopurulent vaginal discharge is the most common symptom, although lower abdominal pain may also be present. Rare cause of intermenstrual bleeding or menorrhagia.
  • Urethral infection - cause of dysuria without frequency.
  • Rectal infection (in women, may develop by spread of infected genital secretions or anal intercourse) - usually asymptomatic.
  • Pharyngeal infection - usually asymptomatic
  • Easily induced contact bleeding of the endocervix.
  • Normal examination (very common).
274
Q

What is the treatment for gonorrhoea?

A

ceftriaxone - IM

also azithromycin for chlamydia

275
Q

What kind of organism is Herpes Simplex Virus?

A

encapsulated
double stranded
DNA

276
Q

What type of infections does HSV-1 cause?

A

oral - cold sores

genital herpes

277
Q

What type of infections does HSV-2 cause?

A

anogenital infection

278
Q

Describe the symptoms of a primary HSV infection

A

May be asymptomatic!
o Febrile flu-like symptoms for 5-7 days. Myalgia and fever are the main systemic symptoms.
o Tingling neuropathic pain in the genital area/buttocks/legs.
o Extensive painful crops of blisters/ulcers in the genital area (including the vagina and cervix in women and the urethra in men).
o Lesions are usually bilateral in primary disease (usually unilateral in recurrent cases).
o Tender lymph nodes (inguinal). Usually bilateral in primary disease.
o Local oedema.
o Dysuria.
o Vaginal or urethral discharge.

279
Q

How does a recurrent HSV infection occur?

A

Following primary infection, the virus becomes latent in local sensory ganglia near to the skin.

280
Q

What are the symptoms of a recurrent HSV infection?

A

lesions - virus travels from ganglia to skin. VERY INFECTIOUS
often unilateral

281
Q

What is the treatment for herpes?

A

aciclovir

282
Q

What organism causes genital warts?

A

HPV

283
Q

What kind of organism is HPV?

A

double stranded

DNA

284
Q

Which types of HPV most commonly cause genital warts?

A

6

11

285
Q

Which types of HPV are associated with a high risk of neoplastic transformation?

A

16

18

286
Q

Describe the clinical presentation of genital warts

A

painless lesions
itching
bleeding

287
Q

What is the treatment for genital warts?

A

o None – frequent spontaneous resolution

o Topical podophyllin, cryotherapy, intralesional interferon

288
Q

Describe the presentation of primary syphilis

A

incubation period 2-3 weeks.
Local infection.
small, painless papule rapidly forms an ulcer = the chancre.

289
Q

Describe the presentation of secondary syphilis

A
incubation period 6-12 weeks. 
Generalized infection, 
night time headaches, 
malaise, 
slight fever 
aches. 
generalized polymorphic rash often affects the palms, soles and face
290
Q

Describe the chancre that appears in primary syphilis

A
round or oval
painless, 
urrounded by a bright red margin, 
indurated with a clean base 
discharging clear serum.
291
Q

What defines whether latent syphilis is early or late?

A

early = asymptomatic for less than 2 years

late = asymptomatic for more than 2 years

292
Q

Describe the presentation of tertiary syphilis

A

cardiovascular syphilis, neurosyphilis,

gummatous syphilis

293
Q

What is the treatment for syphilis?

A

penicillin

294
Q

What kind of organism is Trichomonas vaginalis?

A

protozoa

flagellated

295
Q

Describe the presentation of trichomonas vaginitis in women

A

o vaginal discharge - usually a frothy yellowish discharge
o vulval itching,
o dysuria
o offensive odour
o Lower abdominal discomfort can occur in some women.
o There may be signs of local inflammation with vulvitis and vaginitis.
o Cervicitis may be present which leads to the cervix having the appearance of the surface of a strawberry; sometimes referred to a ‘strawberry cervix’.

296
Q

Describe the presentation of trichomonas infection in men

A

o usually asymptomatic.
o dysuria
o urethral discharge.
o The vast majority of men will have no abnormal signs on examination.

297
Q

What is the treatment for a trichomonas infection?

A

metronidazole

298
Q

What are the risk factors for a vaginal Candida infection?

A
Pregnancy, 
Diabetes mellitus, 
Treatment with broad-spectrum antibiotics (occurs in 28-33%), 
Chemotherapy, 
Vaginal foreign body, 
Contraceptives.
299
Q

Describe the clinical presentation of candidiasis

A
  • Pruritus vulvae = itchiness of the vulva
  • Vulval soreness.
  • White, ‘cheesy’ discharge. The discharge is non-offensive.
  • Dyspareunia - difficult or painful sexual intercourse(superficial).
  • Dysuria (external).
  • Vulval erythema, possibly with fissuring.
  • Vulval oedema.
  • Satellite lesions.
300
Q

What is the treatment for a Candida infection?

A

• Topical azoles or nystatin,

oral fluconazole

301
Q

What causes bacterial vaginosis?

A

overgrowth of predominantly anaerobic organisms in the vagina.
These replace lactobacilli
The pH increases from less than 4.5 to as high as 6.

302
Q

Describe the clinical presentation of bacterial vaginosis

A
  • Offensive, fishy-smelling vaginal discharge without soreness or irritation.
  • Approximately half of all women infected are asymptomatic.
  • On examination there is usually a thin layer of white discharge covering the vaginal wall
303
Q

What is the treatment for a bacterial vaginosis?

A

metronidazole

304
Q

What is pelvic inflammatory disease?

A

The result of infection ascending from the endocervix, causing endometritis, salpingitis, parametritis, oophoritis, tubo-ovarian abscess and/or pelvic peritonitis

305
Q

What are complications of PID?

A
inflammation -> damaged epithelium -> adhesions
infertility
ectopic pregnancy
tubo-ovarian abscess formation
chronic pelvic pain
peri-hepatitis
Reiter's syndrome
preterm delivery
maternal and fetal mortality
306
Q

What organisms can PID be caused by?

A

Chlamydia trachomatis
Neisseria gonorrhoeae
Gardnerella vaginalis
Mycoplasma hominis

307
Q

What are the risk factors for PID?

A
  • Risk factors for acquiring sexually transmitted infections - eg, young age, new sexual partner, multiple sexual partners, lack of barrier contraception, lower socio-economic group.
  • There may be an increased risk in those women who have had an intrauterine contraceptive device (IUCD) inserted in the previous 20 days.
  • Termination of pregnancy.
308
Q

Describe the clinical presentation of PID

A
  • Bilateral lower abdominal pain.
  • Deep dyspareunia - difficult or painful sexual intercourse
  • Abnormal vaginal bleeding (postcoital, intermenstrual or menorrhagia).
  • Vaginal or cervical discharge that is purulent.
  • Lower abdominal tenderness (usually bilateral).
  • Mucopurulent cervical discharge and cervicitis seen on speculum examination.
  • Cervical motion tenderness and adnexal tenderness on bimanual vaginal examination.
  • Fever above 38°C (but may be apyrexial).
  • Nausea or vomiting, urinary symptoms, proctitis and an adnexal mass.
309
Q

How is PID managed?

A

pain relief

outpatient - oral doxycycline and metronidazole

inpatient - IM ceftriaxone

310
Q

Which bones form the pelvic gridle?

A

hip bones
sacrum
coccyx

311
Q

State the attachments of the sacrospinous ligament

A

sacrum

ischial spine

312
Q

State the attachments of the sacrotuberous ligament

A

sacrum

ischial tuberosity

313
Q

How is the gynecoid pelvis different to the android pelvis?

A
  • wider and broader structure
  • lighter in weight
  • An oval-shaped pelvic inlet compared with the heart-shaped android pelvis.
  • Less prominent Ischial spines, allowing for a greater bispinous diameter
  • A greater angled sub-pubic arch, more than 80-90 degrees.
  • sacrum shorter, more curved and with a less pronounced sacral promontory.
314
Q

Describe a good pelvis for childbirth

A
o	Round inlet
o	Straight side walls
o	Ischial spines not too prominent
o	Well-rounded greater sciatic notch
o	Well-curved sacrum (to fit with foetal head)
o	Sub-pubic arch > 900
315
Q

State the boundaries of the pelvic inlet

A
  • Posterior: The sacral promontory (the superior portion of the sacrum).
  • Lateral: The arcuate line on the inner surface of the ilium, and the pectineal line on the superior ramus.
  • Anterior: The pubic symphysis.
316
Q

What separates the greater and lesser pelvis?

A

pelvic inlet

317
Q

Where is the pelvic outlet located?

A

end of the lesser pelvis

beginning of the pelvic wall

318
Q

State the boundaries of the pelvic outlet

A
  • Posterior: The tip of the coccyx
  • Lateral: The ischial tuberosities and the inferior margin of the sacrotuberous ligament
  • Anterior: The pubic arch (the inferior border of the ischiopubic rami).
319
Q

Where is the sub-pubic angle found?

A

The angle beneath the pubic arch

320
Q

State two measurements that are used to assess the lesser pelvis

A
  1. Obstetric Conjugate
    determines the narrowest fixed distance that the foetus would have to negotiate
    This is the distance between the sacral promontory and the midpoint of the pubic symphysis.
  2. Diagonal Conjugate
    measure manually via the vagina the distance from the inferior border of the pubic symphysis to the sacral promontory
321
Q

Why can the obstetric conjugate measurement not be taken clinically?

A

the presence of the bladder

322
Q

How is the diagonal conjugate measured?

A

use the tip of your middle finger to measure the sacral promontory
use the other hand to mark the level of the inferior margin of the pubic symphysis on the examining hand.
You then use the distance between the index finger and the pubic symphysis to measure the obstetric conjugate, ideally 11cm or greater

323
Q

What shape is the pelvic floor?

A

funnel shaped

324
Q

Name the two holes in the pelvic floor

A

urogenital hiatus

rectal hiatus

325
Q

What lies between the urogenital hiatus and the rectal hiatus?

A

perineal body

326
Q

What is the role of the pelvic floor?

A
  • Support of abdominopelvic viscera (bladder, intestines, uterus etc.) through their tonic contraction.
  • Resistance to increase in intra-pelvic/abdominal pressure during activities such as coughing or lifting heavy objects.
  • Urinary and fecal continence. The muscle fibres have a sphincter action on the rectum and urethra.

Separates the pelvic cavity and the perineum

327
Q

State the anatomical borders of the perineum

A
  • Anterior – Pubic symphysis.
  • Posterior– The tip of the coccyx.
  • Laterally – Inferior pubic rami and inferior ischial rami, and the sacrotuberous ligament.
  • Roof – The pelvic floor.
  • Base – Skin and fascia.
328
Q

What separates the perineum into the urogenital and anal triangles?

A

a theoretical line drawn transversely between the ischial tuberosities.

329
Q

State the surface borders of the perineum

A
  • Anteriorly: Mons pubis in females, base of the penis in males.
  • Laterally: Medial surfaces of the thighs.
  • Posteriorly: Superior end of the intergluteal cleft.
330
Q

What is the deep perineal pouch?

A

A potential space between the pelvic floor superiorly, and the perineal membrane inferiorly
found in the urogenital triangle

331
Q

What does the deep perineal pouch contain?

A

part of the urethra
external urethral sphincter

In males, it also contains the the bulbourethral glands and the deep transverse perineal muscles.

332
Q

What is the perineal membrane?

A

A layer of tough fascia, which is perforated by the urethra and vagina.
separates the deep and superficial perineal pouches
found in the urogenital triangle

333
Q

what does the urogenital triangle have that the anal triangle doesn’t?

A

perineal membrane

334
Q

What is the function of the perineal membrane?

A

provide attachment for the muscles of the superficial external genitalia
help support the pelvic viscera

335
Q

What is the superficial perineal pouch?

A

A potential space between the perineal membrane superiorly, and the perineal fascia inferiorly

336
Q

What does the superficial perineal pouch contain?

A

erectile tissues that form the penis and clitoris
ischiocavernosus
bulbospongiosus
superficial transverse perineal muscles.
Bartholin’s glands

337
Q

What is the deep perineal fascia?

A

Fascia covering the superficial perineal muscles.

338
Q

What is the superficial perineal fascia?

A

layer of fascia continuous with the superficial fascia of the abdominal wall.

339
Q

State the components of the anal triangle

A
  • Anal aperture – the opening of the anus.
  • External anal sphincter muscle – voluntary muscle responsible for opening and closing the anus.
  • Two ischioanal fossae – spaces located laterally to the anus.
340
Q

What do the ischioanal fossae contain?

A

fat

connective tissue

341
Q

Where do the ischioanal fossae extend to?

A

the pelvic diaphragm superiorly

the skin of the anal region inferiorly

342
Q

Describe the innervation of the levator ani muscles

A

pudendal nerve, roots S2, S3 and S4.

343
Q

State the component muscles of the levator ani medial to lateral

A

puborectalis,
pubococcygeus
iliococcygeus.

344
Q

State the attachments of the levator ani muscles

A
  • Anterior – The pubic bodies
  • Laterally – Thickened fascia of the obturator internus muscle, known as the tendinous arch.
  • Posteriorly – The ischial spines
345
Q

What is the function of the puborectalis?

A

maintain faecal continence

relaxes during defecation

346
Q

Describe the innervation of the coccygeus

A

anterior rami S4 and S5

347
Q

Describe the position of the coccygeus in relation to the levator ani

A

posterior to levator ani

348
Q

What is the function of the perineal body?

A

joins the pelvic floor to the perineum
tear resistant body between the vagina and the external anal sphincter,
supports the posterior part of the vaginal wall against prolapse

349
Q

Why does prolapse occur?

A

trauma to pelvic floor

poor muscular tone of pelvic floor

350
Q

What are the risk factors for prolapse?

A
  • old age
  • high number of vaginal deliveries
  • Family history of pelvic floor dysfunction
  • large weight
  • Chronic coughing (e.g from a lung disorder)
351
Q

How can the pelvic floor be strengthened?

A

pelvic floor exercises
squeeze and hold the muscles 10 to 15 times in a row. (the muscles used to stop the flow of urine when you go to the toilet)
Do not hold your breath or tighten your stomach, buttock or thigh muscles at the same time.

352
Q

What structures does the perineal body act as an attachment for?

A
  • Levator ani (part of the pelvic floor).
  • Bulbospongiosus muscle.
  • Superficial and deep transverse perineal muscles.
  • External anal sphincter muscle.
  • External urethral sphincter muscle fibres.
353
Q

What are the risk factors for pelvic floor dysfunction?

A

• pregnancy and vaginal delivery
o stretch of pudendal nerve
o stretch of pelvic floor and perineal muscles
o stretch/rupture of supporting ligaments
• hysterectomy
• Increasing age
• Increasing parity
• Overweight (BMI 25-30) and obesity (BMI >30)
• Menopause
• Chronic cough
• Intrinsic connective tissue laxity

354
Q

What is the cause of urinary stress incontinence?

A

pelvic floor muscles are weakened
if there is sudden extra pressure within abdomen and on the bladder, the pelvic floor muscles cannot support the bladder and urethra as well as they should.
The pressure is too much to withstand and so urine leaks out.

355
Q

Describe surgical interventions for pelvic floor dysfunction

A

Colposuspension
= lifting up the neck of your bladder, and stitching it in this lifted position. This can help prevent involuntary leaks in women with stress incontinence.
Tension-free vaginal tape
= plastic tape is inserted through an incision inside the vagina and threaded behind the urethra. By holding the urethra up in the correct position, the piece of tape can help reduce the leaking of urine associated with stress incontinence

356
Q

Which organism is related to squamous neoplastic lesions of the vulva?

A

HPV 16

357
Q

How do squamous neoplastic lesions of vulva present?

A

keratotic warty ulcerated lesions

358
Q

Where do squamous neoplastic lesions of the vulva spread to?

A

inguinal, pelvic, iliac and para-aortic lymph nodes

lungs and liver

359
Q

How are squamous neoplastic lesions of the vulva treated?

A

vulvectomy

lymphadenopathy

360
Q

Why is cervical carcinoma suitable for screening?

A
  • Cervix accessible to visual examination (colposcopy) and sampling = test criteria
  • Slow progression from precursor lesions to invasive cancers (years) = disease criteria
  • Papanicolaou (Pap) test detects precursor lesions and low stage cancers = test criteria
  • Allows early diagnosis and curative therapy = treatment criteria
361
Q

What happens in cervical screening?

A

cells from the transformation zone are scraped off, stained with Papanicolaou stain and examined microscopically
If the test is abnormal the patient is referred for colposcopy and biopsy.

362
Q

Who is screened for cervical cancer?

A

Screening starts age 25 and continues every 3 years until the woman turns 50 and every 5 years for those aged 50-65.

363
Q

Which organism is related to cervical carcinoma?

A

HPV 16

HPV 18

364
Q

How does HPV lead to carcinoma formation?

A

produce viral proteins E6 & E7 which interfere with the activity of tumour suppressor proteins
cause inability to repair damaged DNA and increased proliferation of cells.

365
Q

What are the risk factors for cervical carcinoma?

A
  • Sexual intercourse
  • Early first marriage
  • Early first pregnancy
  • Multiple births
  • Many partners
  • Promiscuous partner
  • Long term use of OCP
  • Partner with carcinoma of the penis – also caused by HPV
  • Low socio-economic class
  • Smoking
  • Immunosuppression – HPV remains in cells
366
Q

What is CIN?

A

Cervical Intraepithelial Neoplasia

= Dysplasia of squamous cells within the cervical epithelium, induced by infection with high risk HPVs

367
Q

Describe the types of CIN

A
  • CIN I – most regresses spontaneously, only a small percentage progresses to further stages
  • CIN II
  • CIN III (carcinoma in situ) – 10% progresses to invasive carcinoma in 2-10 years, 30% regresses
368
Q

How long does the progression form CIN I to CIN II take?

A

7 years

369
Q

What are the treatment options for CIN?

A
  • CIN I – follow-up or cryotherapy

* CIN II & CIN III – superficial excision (cone, large loop excision of the transformation zone (LLETZ))

370
Q

What is the average age of cervical carcinoma?

A

45

371
Q

What type of cancer are most cervical carcinomas?

A

squamous cell - 80%

adenocarcinomas -15%

372
Q

Where do cervical carcinomas spread to?

A

– Locally to para-cervical soft tissues, bladder, ureters, rectum, vagina
– Lymph nodes – para-cervical, pelvic, para-aortic

373
Q

How does cervical carcinoma present?

A

screening abnormality

postcoital, intermenstrual or postmenopausal vaginal bleeding

374
Q

What is the treatment for microinvasive cervical carcinomas?

A

cervical cone excision

375
Q

What is the treatment for invasive cervical carcinomas?

A

hysterectomy,
lymph node dissection
if advanced, radiation and chemotherapy

376
Q

What is endometrial carcinoma associated with?

A

prolonged oestrogentic stimulation:
• Annovulation
• Increased oestrogen from endogenous sources (e.g., adipose tissue)
• Exogenous oestrogen

377
Q

Which type of cancer is most common in the endometrium?

A

adenocarcinoma

378
Q

What age is Endometrial adenocarcinoma most common?

A

55-75

379
Q

How does endometrial carcinoma present?

A

irregular or postmenopausal vaginal bleeding

380
Q

Describe the features of Endometrioid Endometrial Adenocarcinoma

A
  • Typically arises in setting of endometrial hyperplasia
  • Mimics proliferative glands
  • Associated with unopposed oestrogen and obesity
381
Q

How does Endometrioid Endometrial Adenocarcinoma spread?

A

myometrial invasion

direct extension to adjacent structures, to local lymph nodes and distant sites

382
Q

Describe the features of Serous Endometrial Adenocarcinoma

A

• Poorly differentiated, aggressive, worse prognosis

383
Q

How does Serous Endometrial Adenocarcinoma spread?

A

Exfoliates, travels through Fallopian tubes, implants on peritoneal surfaces

384
Q

What is a leiomyoma?

A

fibroid!

Benign tumour of myometrium

385
Q

describe the presentation of leiomyoma

A

asymptomatic
can cause heavy/painful periods, urinary frequency (bladder compression), infertility
round firm and whitish

386
Q

When is uterine leiomyosarcoma most common?

A

40-60 years

387
Q

Where does uterine leiomyosarcoma metastasise to?

A

lungs

388
Q

What proportion of ovarian tumours are benign?

A

80%

389
Q

What age do benign tumours of the ovary present?

A

20-45

390
Q

What age do malignant tumours of the ovary present?

A

45-65

391
Q

Why is prognosis of ovarian cancer poor?

A

often spread beyond the ovary at time of presentation - when they become large, invade adjacent structures or metastasize

392
Q

Where do ovarian cancers spread to?

A

regional nodes and elsewhere e.g., liver, lungs

Approximately 50% spread to other ovary

393
Q

What tumour marker is used in ovarian cancer?

A

serum CA-125

394
Q

What are the risk factors for ovarian epithelial tumours?

A
  • Nulliparity or low parity
  • OCP protective
  • Heritable mutations, e.g., BRCA1 and BRCA2
  • Smoking
  • Endometriosis
395
Q

State the three types of ovarian epithelial tumour

A

serous
mucinous
endometrioid

396
Q

Why are serous ovarian epithelial tumours associated with ascites?

A

Often spread to peritoneal surfaces and omentum,

397
Q

What are the features of mucinous ovarian epithelial tumours?

A

large, cystic masses – can be >25kg
Filled with sticky, thick fluid
Usually benign or borderline

398
Q

What are the features of endometrioid ovarian epithelial tumours?

A

Contain tubular glands resembling endometrial glands
Can arise in endometriosis (15-20% of cases)
15-30% have associated endometrial endometrioid adenocarcinoma, probably arising separately

399
Q

What tumour marker is found in non-gestational choriocarcinoma of the ovaries?

A

hCG

400
Q

What tumour marker is found in a yolk sac tumour of the ovaries?

A

α-fetoprotein

401
Q

What are the features of mature ovarian teratomas?

A

dermoid cysts!
benign
contain skin-like structures
Usually contain hair and sebaceous material, can contain tooth structures
Often tissue from other germ layers also present

402
Q

What are the features of immature ovarian teratomas?

A

malignant

composed of tissues that resemble immature foetal tissue

403
Q

What are the features of the two types of monodermal ovarian teratomas?

A

– Struma ovarii
• Benign
• Composed entirely of mature thyroid tissue
• May be functional and cause hyperthyroidism
– Carcinoid
• Malignant
• May be functional producing 5HT and can cause carcinoid syndrome (even without hepatic metastases!)

404
Q

Where are Ovarian Sex Cord-Stromal Tumours derived from?

A

ovarian stroma

405
Q

What cell types can be found in Ovarian Sex Cord-Stromal Tumours?

A

Sertoli and Leydig cells

granulosa and theca cells

406
Q

Which tumours most commonly metastasise to the ovaries?

A
–	Uterus
–	Fallopian tubes
–	Contralateral ovary
–	Pelvic peritoneum
Also gastrointestinal tumours (colon, stomach, biliary tract, pancreas, appendix) and breast
407
Q

What is Gestational Trophoblastic Disease?

A

= Tumours and tumour-like conditions which show proliferation of placental
tissue

408
Q

What is Hydatidiform Mole?

A

Cystic swelling of chorionic villi and trophoblastic proliferation
Friable mass of thin-walled, translucent, grape-like structures = swollen oedematous villi

409
Q

How does hydratidiform mole present?

A

abnormality on ultrasound scan

miscarriage

410
Q

Who is most at risk of Hydatidiform Mole?

A

teenagers

40-50

411
Q

How is Hydatidiform Mole treated?

A

curettage

hCG monitoring

412
Q

What is an invasive mole?

A
  • Mole that penetrates or perforates uterine wall

* Locally destructive – can cause uterine rupture requiring hysterectomy

413
Q

How does invasive mole present?

A

vaginal bleeding
uterine enlargement
persistently elevated hCG

414
Q

How is Invasive Mole treated?

A

chemotherapy

415
Q

What is a gestational choriocarcinoma?

A

Malignant neoplasm of trophoblastic cells derived from previously normal or abnormal pregnancy

416
Q

How does gestational choriocarcinoma present?

A

vaginal spotting

high hCG levels

417
Q

How is gestational choriocarcinoma treated?

A

uterine evacuation and chemotherapy

418
Q

Define adrenarche

A

bodily process that happens between the ages of 6 and 8.
androgens begin to increase and may go unnoticed or can cause pubic hair growth and increased secretion from sebaceous glands.
In girls, the androgens are secreted by the adrenal glands.

419
Q

Define thelarche

A

onset of female breast development

dependent on oestrogen

420
Q

define pubarche

A

first onset of pubic hair

421
Q

Define menarche

A

first menstrual cycle in female

422
Q

Define spermarche

A

beginning of development of sperm in boys’ testicles at puberty

423
Q

What is the Tanner Standard?

A

a way to classify pubertal development

424
Q

In males, what factors are used to measure the Tanner Standard?

A
testicular volume, 
penis enlargement, 
pubic hair, 
axillary hair
spermarche
425
Q

In females, what factors are used to measure the Tanner Standard?

A

breast size,
pubic hair growth,
axillary hair growth
menarche

426
Q

When does male puberty begin?

A

9-14 years

427
Q

When does female puberty begin?

A

8-13

428
Q

What is the first sign of puberty in females?

A

thelarche - breast bud forming

429
Q

What is the rate of growth in cm/yr in puberty?

A

males: 10.3
females: 9

430
Q

Which hormones initiate puberty?

A

rise in pulsatile GnRH
increase freq and amp of nocturnal LH pulses
sex steroids released

elevation of IGF-1, adrenal steroids, GH and TSH

431
Q

What does the rise in puberty of LH and FSH in males cause?

A

initiates spermatogenesis and androgen secretion from the testes
Androgens initiate the growth of sex accessory structures and male secondary sexual characteristics.
The androgens also cause retention of minerals in the body to support bone and muscle growth.

432
Q

What does the rise in puberty of LH and FSH in females cause?

A

Oestrogen induces the secondary sex characteristics, such as:
growth of the pelvis
deposition of subcutaneous fat
growth of internal reproductive organs and external genitalia.

The androgens released by the adrenal glands initiate growth of pubic hair, lowering of the voice, bone growth and increased secretion from sebaceous glands.

433
Q

What weight initiates menarche?

A

47kg = critical weight

434
Q

What causes the growth spurt to end?

A

oestrogen

closes epiphyseal growth plates

435
Q

Before what age is puberty considered precocious?

A

males: 9
females: 8

436
Q

What causes gonadotropin dependent precocious puberty?

A

Hormone secreting tumours eg. pineal tumours, germ cell tumours

437
Q

What causes gonadotropin independent precocious puberty?

A

 Early stimulation of central maturation
 Meningitis or trauma leads to prevention of GnRH inhibition so GnRH is secreted by the hypothalamus
 Congenital adrenal hyperplasia
 HCG secreting tumours in the liver
 Adrenal tumours
 Testotoxicosis
 Exogenous oestrogen or androgen exposure

438
Q

Define precocious puberty

A

appearance of secondary sexual characteristics due to increased hormone production occurring independently to the HPG axis.

439
Q

Describe the hormone levels in precocious puberty

A

low LH and FSH

high testosterone/oestrogen

440
Q

When is puberty considered delayed?

A

initial physical changes have not appeared by

males: 14
females: 13

or >5year interval between first signs and completion

441
Q

What are the causes of delayed puberty?

A
•	Gonadal Failure
Turner’s syndrome
Post malignancy
Polyglandular autoimmune syndromes
•	Gonadal deficiency
Congenital hypogonadotrophic hypogonadism
Hypothalamic/pituitary lesion
Genetic mutations inactivating FSH/LH or their receptors
442
Q

When does pre-menopause occur?

A

after 40

443
Q

What happens to the hormonal levels in pre-menopause?

A

less oestrogen secreted
less -ve feedback so more LH and FSH
loss of inhibin so FSH rises more

444
Q

What happens to the menstrual cycle in pre-menopause?

A

follicular phase shortens

ovulation early or absent

445
Q

Define menopause

A

Cessation of menstrual cycles for a clear 12 months

446
Q

When does menopause occur?

A

49-50

447
Q

What happens to the hormonal levels in menopause?

A

oestrogen levels fall dramatically
less -ve feedback so more LH and FSH
loss of inhibin so FSH rises dramatically

448
Q

What are the effects of menopause on the vascular system?

A

Hot flushes

449
Q

What are the effects of menopause on oestrogen sensitive tissues?

A
o	Uterus
Regression of endometrium
Srinkage of myometrium
o	Thinning of cervix
o	Vaginal rugae lost
Thinner, less distensible
o	Involution of some breast tissue
o	Changes in skin
o	Reduction in bladder tone, leading to urinary incontinence
450
Q

What are the effects of menopause on bone?

A

Reduced Oestrogen enhances osteoclast activity
Increased reabsorption relative to production

Osteoporosis!

451
Q

What are the advantages of HRT?

A

relieves symptoms of the menopause

can limit osteroporosis

452
Q

What are the disadvantages of HRT?

A

breast and ovarian cancer risk

453
Q

Define amenorrhoea

A

absence of periods for at least 6 months

454
Q

Distinguish between primary and secondary amenorrhoea

A

primary = never had a period. Absence of menses by age 14 with absence of Secondary Sexual Characteristics (SSC)

Secondary = established menstruation has ceased

455
Q

Define oligomenorrhoea

A

Infrequent periods occurring at intervals of 35 days – 6 months

456
Q

define dysmenorrhoea

A

painful periods

457
Q

define menorrhagia

A

Heavy periods. Excessive (>80ml), prolonged (> 7 day) uterine bleeding

usually secondary to distortion of the uterine cavity

458
Q

define Cryptomenorrhoea

A

Periods occur but not visible due to obstruction in outflow tract

459
Q

What is the hormonal reason for hypothalamic/pituitary amenorrhoea?

A

Inadequate levels of FSH lead to inadequately stimulated ovaries,
overies fail to produce enough oestrogen to stimulate the endometrium of the uterus, giving amenorrhoea

460
Q

What are some disease states that cause hypothalamic/pituitary amenorrhoea?

A

o Primary Hypothalamic Amenorrhoea
Kallmann Syndrome – Inability to produce GnRH (& FSH subsequently)
o Secondary Hypothalamic Amenorrhoea
Exercise Amenorrhoea – Related to physical exercise
Stress Amenorrhoea
Eating disorders and weight loss (Obesity, anorexia or bulimia). Fall below critical weight of 47kg menses will cease
o Secondary Pituitary Amenorrhoea
Sheehan syndrome – Hypopituitarism
Hyperprolactinaemia
Haemochromatosis – ‘Iron overload’

461
Q

What is the hormonal reason for gonadal/end-organ amenorrhoea?

A

the ovary does not respond to pituitary stimulation, giving low oestrogen levels.
The lack of –‘ve feedback from oestrogen leads to elevated FSH levels in the menopausal range

462
Q

What are some disease states that cause gonadal/end-organ amenorrhoea?

A
o	Primary Gonadal/End-Organ
Gonadal dysgenesis – E.g. Turner Syndrome (45, X)
Androgen Insensitivity Syndrome
Receptor abnormalities for FSH and LH
Specific forms of congenital adrenal hyperplasia
o	Secondary Gonadal/End-Organ
Pregnancy
Anovulation
Menopause (Or premature menopause)
Polycystic Ovarian Syndrome
Drug-induced
463
Q

Define Dysfunctional Uterine Bleeding (DUB)

A

irregular uterine bleeding that occurs in the absence of recognizable pelvic pathology, general medical disease, or pregnancy.
A diagnosis of exclusion

464
Q

Explain how the hormonal levels in DUB lead to the symptoms

A

constant, noncycling estrogen levels that stimulate endometrial growth
Proliferation without periodic shedding causes the endometrium to outgrow its blood supply
tissue breaks down and sloughs from the uterus.

465
Q

Describe the arterial supply of the scrotum

A

anterior scrotal artery - from external pudendal

posterior scrotal artery - from internal pudendal

466
Q

Describe the venous drainage of the scrotum

A

scrotal veins - into external pudendal

467
Q

Describe the cutaneous innervation of the scrotum

A

anterolateral aspect = Genital branch of genitofemoral nerve – derived from the femoral plexus

anterior aspect = Anterior scrotal nerves – derived from the ilioinguinal nerve

posterior aspect = Posterior scrotal nerves – derived from the perineal nerve

inferior aspect = Perineal branches of posterior femoral cutaneous nerve – derived from the sacral plexus

468
Q

Where does lymph fluid fro the scrotum drain to?

A

superficial inguinal nodes

469
Q

What is a hydrocele?

A

a collection of serous fluid within the tunica vaginalis.

most commonly due to a failure of the processus vaginalis to close.

470
Q

What is a haematocoele?

A

collection of blood in the tunica vaginalis

471
Q

How can we tell the difference between a haematocoele and a hydrocele?

A

by transillumination

Due to the dense nature of blood, light is unable to pass through.

472
Q

What is a varicocoele?

A

dilation of the veins draining the testes.

473
Q

Which scrotum is a varicocoele more common in?

A

Left

testicular vein drains into left renal vein - smaller and at an acute angle

474
Q

Where is the epididymis positioned within the scrotum?

A

posterolateral aspect

475
Q

Describe the innervation of the testes and epididymis

A

testicular plexus – a network of nerves derived from the renal and aortic plexi.

476
Q

Describe the arterial supply of the testes and epididymis

A

paired testicular arteries
arise directly from the abdominal aorta.
pass into the scrotum via the inguinal canal, contained within the spermatic cord

477
Q

Describe the venous drainage of the testes and epididymis

A

pampiniform plexus in the scrotum
paired testicular veins
left testicular vein drains into the left renal vein,
right testicular vein drains directly into the inferior vena cava.

478
Q

Describe the lymphatic drainage of the testes and epididymis

A

paired lumbar and preaortic nodes, located at the L1 vertebral level.

479
Q

Describe the route of the spermatic cord

A

formed at the deep inguinal ring, laterally to the inferior epigastric vessels.
passes through the inguinal canal, entering the scrotum via the superficial inguinal ring.
continues into the scrotum, ending at the posterior border of the testes.

480
Q

State the fascial layers of the spermatic cord

A

External spermatic fascia
Cremasteric muscle
Internal spermatic fascia

481
Q

State which layers of the anterior abdominal wall the fascial layers of the spermatic cord are derived from

A
  • External spermatic fascia – aponeurosis of the external oblique.
  • Cremasteric muscle and fascia – internal oblique and its fascial coverings.
  • Internal spermatic fascia – transversalis fascia
482
Q

State the afferent an efferent limbs of the cremasteric reflex

A

afferent - ilioiguinal or genitofemoral nerve

efferent - genital branch of the genitofemoral nerve

483
Q

How is the cremasteric reflex stimulated?

A

stroking the superior and medial part of the thigh.

484
Q

What is the response in the cremasteric reflex?

A

contraction of the cremasteric muscle, elevating the testis on the side that has been stimulated.

485
Q

What runs within the spermatic cord?

A
  • Testicular artery
  • Cremasteric artery and vein
  • Artery to the vas deferens – a branch of the inferior vesicle artery, which arises from the internal iliac.
  • Pampiniform plexus of testicular veins
  • Genital branch of the genitofemoral nerve
  • Vas deferens
  • Lymph vessels
  • Processus vaginalis
  • Autonomic nerves
486
Q

Where do the testicular arteries arise?

A

from the aorta just inferiorly to the renal arteries.

487
Q

Why is testicular torsion a medical emergency?

A

occlusion of the testicular artery,

necrosis of the testes.

488
Q

What are the symptoms of testicular torsion?

A

severe, sudden pain in one or both of the testes, where the onset is often during exercise or physical activity

489
Q

Describe the anatomical course of the vas derferens

A

continuous with the tail of the epididymis.
Ascends in spermatic cord
Travels through the inguinal canal.
Moves down the lateral pelvic wall in close proximity to the ischial spine.
Turns medially to pass between the bladder and the urethra.
Forms dilated ampulla
Joins the duct from the seminal vesicle to form the ejaculatory duct.

490
Q

Where are the seminal vesicles located?

A

between the bladder fundus and the rectum

491
Q

Which structures are derived from the mesonephric ducts?

A

Seminal glands,
Ejaculatory ducts,
Epididymis
Ductus (vas) deferens

492
Q

Branches from which artery supply the seminal glands?

A

internal iliac artery

493
Q

Describe the lymphatic drainage of the seminal vesicles

A

external and internal iliac lymph nodes

494
Q

What is a complication of a seminal gland abscess?

A

rupture

pus enters peritoneal cavity

495
Q

How can swollen seminal glands be detected?

A

DRE

496
Q

Describe the location of the prostate gland

A

inferior to the neck of the bladder
superior to the external urethral sphincter,
levator ani muscle lies inferolaterally to the gland

497
Q

State the three histological zones of the prostate gland

A

Central zone
Transitional zone
Peripheral zone

498
Q

State the embryological origin of the zones of the prostate gland

A
  • Central zone – the Wolffian duct.
  • Transitional zone – the urogenital sinus.
  • Peripheral zone – the Urogenital Sinus.
499
Q

Describe the arterial supply of the prostate

A

prostatic arteries - mainly derived from the internal iliac arteries.

500
Q

Describe the venous drainage of the prostate

A

prostatic venous plexus, draining into the internal iliac veins

also connects posteriorly by networks of veins, including the Batson venous plexus, to the internal vertebral venous plexus.

501
Q

Why does prostate cancer spread to the pelvis and vertebrae?

A

drains into Batson venous plexus, which drains to the internal vertebral venous plexus.

502
Q

What is Benign Prostatic Hyperplasia?

A

increase in size of the prostate, without the presence of malignancy.

503
Q

What are the symptoms of BPH?

A

urinary frequency,
urinary urgency
difficulty in initiating micturition

due to compression of bladder and urethra

504
Q

Which zone of the prostate does BPH occur in?

A

transitional zone (central)

505
Q

Which zone of the prostate does prostatic carcinoma occur in?

A

peripheral zones

506
Q

How does a prostatic carcinoma feel on DRE?

A

hard irregular prostate gland.

507
Q

State the three parts of the penis

A

root
body
glans

508
Q

What are the contents of the root of the penis?

A

three erectile tissues (two crura and bulb of the penis)

two muscles (ischiocavernosus and bulbospongiosus).

509
Q

What are the contents of the body of the penis?

A

three cylinders of erectile tissue

two corpus cavernosa, and the corpus spongiosum

510
Q

What are the contents of the glans of the penis?

A

distal expansion of the corpus spongiosum

external urethral orifice

511
Q

What do the crura of the root of the penis continue to form?

A

corpus cavernosa

512
Q

What does the bulb of the root of the penis continue to form?

A

corpus spongiosum

513
Q

Where does the corpus spongiosum lie?

A

ventrally

514
Q

Which erectile tissue does the urethra run through?

A

corpus spongiosum

515
Q

Name the muscles located in the root of the penis

A

Bulbospongiosus (x2)

Ischiocavernosus (x2)

516
Q

What is the function of the bulbospongiosus?

A

contracts to empty the spongy urethra of any residual semen and urine.

anterior fibres also aid in maintaining erection by increasing the pressure in the bulb of the penis.

517
Q

What is the function of the ischiocavernosus?

A

surrounds the left and right crura of the penis.
contracts to force blood from the cavernous spaces in the crura into the corpus cavernosa – this helps maintain erection.

518
Q

Describe the fascia of the erectile tissues of the penis

A

superficial - deep fascia of penis. continuation of deep perineal fascia

deep - tunica albuginea

519
Q

How is the roof of the penis supported?

A

Suspensory ligament – condensation of deep fascia. connects the erectile bodies of the penis to the pubic symphysis.

• Fundiform ligament – condensation of abdominal subcutaneous tissue. It runs down from the linea alba, surrounding the penis like a sling, and attaching to the pubic symphysis.

520
Q

Describe the arterial supply of the penis

A
internal iliac artery ->
internal pudendal artery ->
•	Dorsal arteries of the penis
•	Deep arteries of the penis
•	Bulbourethral artery
521
Q

Describe the venous drainage of the penis

A

deep dorsal vein drains cavernous spaces and empties into the prostatic venous plexus.

The superficial dorsal veins drain the superficial structures of the penis

522
Q

Which spinal segments innervate the penis?

A

S2-S4

523
Q

Describe the innervation of the penis

A

Sensory = dorsal nerve of the penis, a branch of the pudendal nerve.

sympathetic = dorsal nerve of the penis, a branch of the pudendal nerve.

Parasympathetic = cavernous nerves from the prostatic nerve plexus

524
Q

What is phimosis?

A

the prepuce fits tightly over the glans and cannot be retracted.
It can cause irritation when smegma accumulates in the preputial sac.

525
Q

What is the preputial sac?

A

potential space between the glans and prepuce

526
Q

What is the frenulum?

A

median fold of skin on the ventral surface of the penis connected to the prepuce

527
Q

What is paraphimosis?

A

retraction of the prepuce and the glans that constricts the neck of the glans, interfering with venous and lymphatic drainage.
This may cause the glans to enlarge to the extent that the prepuce cannot be drawn over it.

528
Q

What is Peyronie’s Disease?

A

abnormal curvature of the shaft of the penis caused by a build-up of scar tissue.

529
Q

What causes ED?

A
hypertension
hypercholesterolemia
diabetes
anxiety
depression
530
Q

What is priapism?

A

an erection that persists for more than four hours despite a lack of sexual stimulation.
It is often painful and results from blood becoming trapped in the erectile bodies.

531
Q

Which region of the male urethra is most vulnerable to trauma during catheterisation?

A

membranous - least distensible

passes through perineum and pelvic floor

532
Q

What are the ovaries attached to?

A

the posterior surface of the broad ligament of the uterus by the mesovarium - a fold of peritoneum

533
Q

What are the components of the ovary?

A

surface
cortex
medulla

534
Q

Describe the surface of the ovary

A

simple cuboidal epithelium,

535
Q

Describe the cortex of the ovary

A

connective tissue stroma that supports thousands of follicles.

536
Q

Describe the medulla of the ovary

A

inner part

supporting stroma - neurovascular network which enters at the hilum of the ovary

537
Q

What are ovarian cysts?

A

fluid-filled masses, most commonly derived from the ovarian follicles

538
Q

Which ligaments attach to the ovary?

A

suspensory ligament - extends from mesovarium to pelvic wall

ligament of the ovary - from ovary to fundus of uterus.

539
Q

Describe the course of the round ligament of the uterus

A

uterus
inguinal canal
labia majora

540
Q

Describe the arterial supply of the ovaries

A

abdominal aorta

ovarian arteries - arise below renal arteries

541
Q

Describe the venous drainage of the ovaries

A

ovarian veins.

left ovarian vein drains into the left renal vein,
right ovarian vein drains directly into the inferior vena cava.

542
Q

Describe the lymphatic drainage of the ovaries

A

para-aortic nodes

543
Q

which ligament do the fallopian tubes lie within?

A

upper border of broad ligament

544
Q

How is the fallopian tube connected to the abdominal cavity?

A

abdominal ostium

545
Q

Describe the arterial supply of the fallopian tubes

A

uterine arteries - from internal iliac

ovarian arteries- from abdominal aorta

546
Q

Describe the venous drainage of the fallopian tubes

A

uterine and ovarian veins

547
Q

Describe the lymphatic drainage of the fallopian tubes

A

liac, sacral and aortic lymph nodes

548
Q

What is salpingitis?

A

inflammation of the uterine tubes that is usually caused by bacterial infection.

549
Q

What are the potential consequences of salpingitis?

A

adhesions of mucosa
infertility
ectopic pregnancy

550
Q

What are the parts of the uterus?

A

fundus
body
cervix

551
Q

What marks the boundary between the fundus and the body of the uterus?

A

entry of the fallopian tubes

552
Q

What is the normal position of the uterus?

A

anteverted - with respect to vagina

anteflexed - with respect to cervix

553
Q

Define anteverted

A

Rotated forward, towards the anterior surface of the body.

554
Q

Define anteflexed

A

Flexed, towards the anterior surface of the body.

555
Q

which postion of the uterus makes prolapse of the uterus more likely?

A

retroverted

positioned directly above the vagina

556
Q

What hormone causes the stratum functionalis to proliferate?

A

oestrogen

557
Q

What hormone causes the stratum functionalis to become secretory?

A

progesterone

558
Q

Which ligament is a remnant of the gubernaculum?

A

round ligament

559
Q

What is the function of the round ligament of the uterus?

A

to maintains the anteverted position of the uterus.

560
Q

What is the function of the uterosacral ligament of the uterus?

A

provides support to the uterus, opposing the anterior pull of the round ligament.

561
Q

Describe the arterial supply of the uterus and cervix

A

internal iliac artery

uterine artery

562
Q

Describe the venous drainage of the uterus and cervix

A

uterine veins

563
Q

Describe the lymphatic drainage of the uterus

A
body = iliac, sacral
fundus = aortic, inguinal
564
Q

What structure is often damaged during a hysterectomy?

A

ureter

565
Q

What is the relationship between the ureter and the uterine artery?

A

The uterine artery crosses the ureters approximately 1 cm laterally to the internal os

566
Q

What is endometriosis?

A

presence of ectopic endometrial tissue at sites outside the uterus

567
Q

Name the parts of the cervix

A

endocervical canal

ectocervix

568
Q

How is the ectocervix examined?

A

using a speculum

569
Q

Describe the lymphatic drainage of the cervix

A

external and internal iliac nodes

sacral nodes

570
Q

Where are the vaginal fornices found?

A

around the cervix

571
Q

Name the vaginal fornices

A

anterior
lateral x 2
posterior

572
Q

What causes a vaginal fistula?

A

long and traumatic childbirth
the foetus cuts off blood supply
necrosis
open communication between vagina and adjacent pelvic organ

573
Q

State the three main types of vaginal fistulae

A
  • Vesicovaginal – Between the vagina and the bladder. Urine enters the vagina constantly.
  • Urethrovaginal – Between the vagina and the urethra. Urine only enters the vagina during urination.
  • Rectovagina – Between the vagina the rectum. Fecal matter can be enter the vagina in this type of fistula
574
Q

What is vaginisimus?

A

condition making any sort of vaginal penetration (sexual intercourse, insertion of tampons) painful or impossible.
Reflex of the pubococcygeus muscle

575
Q

Describe the arterial supply of the vagina

A

uterine and vaginal arteries, branches of the internal iliac artery.

576
Q

Describe the venous drainage of the vagina

A

vaginal venous plexus, which drains into the internal iliac veins, via the uterine vein.

577
Q

Describe the lymphatic drainage of the vagina

A

iliac and superficial inguinal lymph nodes

578
Q

Describe the innervation of the vagina

A

Inferior 1/5th = Pudendal Nerve (S2-4)

Superior 4/5th = Uterovaginal plexus

579
Q

What are the labia majora derived from?

A

genital swellings

580
Q

What are the labia minora derived from?

A

genital folds

581
Q

What is the clitoris derived from?

A

genital tubercle

582
Q

Describe the arterial supply of the external genitalia

A

pudendal arteries

583
Q

Describe the venous drainage of the external genitalia

A

pudendal veins

584
Q

Describe the lymphatic drainage of the external genitalia

A

superficial inguinal lymph nodes

585
Q

Describe the sensory innervation of the vulva

A

anterior portion = ilioinguinal nerve and the genital branch of the genitofemoral nerve

posterior portion = pudendal nerve and the posterior cutaneous nerve of the thigh.

586
Q

State when the periods of fetal development start and finish.

A

Pre-Embryonic Period = Fertilisation - 3 weeks

Embryonic Period = 3 - 8 weeks

Fetal Period = 8 - 38 weeks

587
Q

What happens during the embryonic period?

A

organs are generated

very little absolute growth

588
Q

What happens during the fetal period?

A

structures created during the embryonic period grow and mature.
Weight gain accelerates.

589
Q

What happens in weeks 8-16 of lung development?

A

Pseudoglandular Stage
The duct systems begin to form within the bronchopulmonary segments created during the embryonic period
Bronchioles are formed

590
Q

What happens in weeks 16-26 of lung development?

A

Canalicular Stage

The respiratory bronchioles are formed due budding from the bronchioles

591
Q

What happens in weeks 26-term of lung development?

A

Terminal Sac Stage
Terminal sacs (alveolar membranes) begin to bud from the respiratory bronchioles
Differentiation of pneumocytes occurs
Type 1 – Gas exchange
Type 2 – Surfactant production from week 20. Significant at 30 weeks

592
Q

What happens from birth to eight years in lung development?

A

Alveolar Period

95% of Alveoli are formed post-natally

593
Q

Why does the fetus make breathing movements?

A

conditions the respiratory musculature

594
Q

When does the fetus begin to move?

A

week 8

595
Q

What is ‘quickening’?

A

Maternal awareness of fetal movements from Week 17 onwards

596
Q

When do the corticospinal tracts begin to develop int eh fetus?

A

16 weeks

597
Q

What is required for coordinated movement of the fetus?

A

myelination of the brain - corticospinal tracts

598
Q

Why is there increased infant mobility within the first year of life?

A

Corticospinal tract myelination is incomplete at birth

myelination occurs in the first year of birth

599
Q

What contributes to the volume of amniotic fluid?

A

fetal urine
fetal lung fluid
placenta and fetal membranes

600
Q

What does fetal kidney dysfunction cause?

A

oligohydraminos = too little amniotic fluid

601
Q

What defines the threshold of viability?

A

terminal sac stage of lung development (after 24 weeks).

602
Q

What causes infant respiratory distress syndrome?

A

insufficient surfactant production because of the small number of type II pneumocytes.

603
Q

How is respiratory distress syndrome alleviated in pre-term delivery?

A

Glucocorticoid treatment to mother

increases surfactant production in the fetus

604
Q

When is a fetus regarded as having growth restriction?

A

its weight is below the 10th percentile for gestational age.

605
Q

What causes oligohydraminos?

A
  • Placental insufficiency
  • Fetal renal impairment
  • Pre-eclampsia
606
Q

What causes polyhydraminos?

A

• Fetal abnormality
inability to swallow
Structural – blind-ended oesophagus
Neurological – unable to coordinate swallowing movements

607
Q

What is symmetrical growth restriction?

A

Growth restriction is generalised and proportional

608
Q

What is asymmetrical growth restriction?

A

fetal abdominal circumference (AC) classically reduced out of proportion to other fetal biometric parameters and is below the 10th percentile

609
Q

What causes asymmetrical growth restriction?

A

malnutrition in weeks 28-term, when the dominant cellular growth mechanism is hypertrophy

610
Q

What causes symmetrical growth restriction?

A

malnutrition in weeks 0-20, when the dominant cellular growth mechanism is hyperplasia.

611
Q

What is the developmental origins of health and disease hypothesis?

A

states that Nutritional and hormonal status during fetal life can influence health in later life

612
Q

What causes Relative sparing of head growth?

A

deprivation of nutritional and oxygen supply to fetus

613
Q

Which metabolic hormone is dominant in the first trimester?

A

IGF II

614
Q

Which metabolic hormone is dominant in the second and third trimesters?

A

IGF I

615
Q

Why does morning sickness not affect fetal growth?

A

experienced in first trimester

IGF II is nutrient independent

616
Q

Why could maternal nutrient status impact the growth of the fetus in the second and third trimester?

A

IGF I is nutrient dependent

617
Q

How does oxygenated blood bypass the liver in the fetus?

Why does this need to happen?

A

ductus venosus

maintain oxygen saturation - the brain needs more oxygen than the liver!

618
Q

How does oxygenated blood pass from the right to the left atrium in the fetus?

A

foramen ovale

619
Q

How is the majority of blood flow in the right atrium directed into the left atrium in the fetus?

A

‘crista dividens’ = free border of the septum secundum

620
Q

Why does the majority of blood flow in the right atrium need to be directed into the left atrium in the fetus?

A

maintain the oxygen saturation.

A minor proportion of blood flows into the right ventricle, mixing with the deoxygenated blood from the SVC

621
Q

How does blood leave the pulmonary artery and enter the aorta in the fetus?

A

ductus arteriosus

622
Q

What is the importance of the ductus arteriosus enters the aorta distal the blood supply of the head?

A

blood in the pulmonary artery is deoxygenated

so that the drop in o2 saturation in minimised

623
Q

What happens to the fetal heart rate in response to hypoxia?

A

heart rate SLOWS

to reduce O2 demand

624
Q

What can chronic fetal hypoxaemia result in?

A

growth restriction and behavioural changes for the child

625
Q

What is the volume of the amniotic sac?

A

10 ml at 8 weeks
1 litre at 38 weeks.
volume decreases post-EDD.

626
Q

Describe the composition of amniotic fluid

A
98% water, 
electrolytes, 
creatinine, 
urea, 
bile pigments, 
renin, 
glucose,
hormones 
fetal cells, 
lanugo 
vernix caseosa (
627
Q

What is lanugo?

A

hair covering the fetus

628
Q

What is vernix caseosa?

A

waxy or cheese-like white substance that protects the skin of the fetus

629
Q

What is the meconium?

What is it composed of?

A

first bowel movement after birth

debris from the amniotic fluid, plus intestinal secretions

630
Q

Why is physiological jaundice common at birth?

A

During gestation, the clearance of fetal bilirubin is handled by the placenta.
The fetus is unable to conjugate bilirubin due to the immaturity of the liver and intestinal processes for metabolism, conjugation and excretion.

631
Q

Why does HbF have a greater affinity for oxygen?

A

doesn’t bind 2,3-BPG as well

632
Q

What is the double Bohr effect?

A

As CO2 passes into the intervillous blood from the fetus, the maternal pH decreases = Bohr effect, decreasing the affinity of maternal Hb for O2

At the same time, as CO2 is lost from the fetal blood, pH rises = Bohr effect, increasing the affinity of fetal Hb for O2

633
Q

How is the pCO2 in maternal blood lowered?

A

Progesterone-driven hyperventilation

634
Q

What is the Haldane effect?

A

Deoxygenated blood can carry increasing amounts of carbon dioxide, whereas oxygenated blood has a reduced carbon dioxide capacity.

635
Q

What is the double Haldane effect?

A

As maternal Hb gives up O2 at the placenta, it can accept increasing amounts of CO2 due to this lower pO2.

Fetus is able to give up more CO2 as O2 is accepted