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Phase 1 revision > SUGER- reproduction > Flashcards

SUGER- reproduction Flashcards

1
Q

What are the pregnancy hormones?

A

1) Human chorionic gonadotropin
2) Oestrogen
3) Progesterone
4) Prolactin
5) Relaxin
6) Oxytocin
7) Prostaglandins

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2
Q

Throughout pregnancy what happens to the plasma conc of oestrogen and progesterone?

A

continuously increases throughout

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3
Q

What is the function of Oestrogen during pregnancy?

A

1) Stimulates the growth of the uterine muscle mass which will eventually produce the contractile force required to deliver the foetus
2) Regulates progesterone levels
3) Prepares the breasts for feeding
4) Induces the synthesis of receptors for the posterior
pituitary hormone, oxytocin, which is a powerful stimulator of uterine muscle contraction

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4
Q

What is the function of progesterone through pregnancy?

A

1) prevents uterine contractions so that foetus is not expelled prematurely
2) Increases the thickness of the uterine lining to prevent miscarriage

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5
Q

where is almost all of the oestrogen &

progesterone supplied by during first 2 months of pregnancy? if pregnancy did not occur then what would have happened?

A

During the first 2 months of pregnancy almost ALL of the oestrogen & progesterone is supplied by the CORPUS LUTEUM (remains for the first 3 months
of pregnancy)
- If pregnancy had not occurred then the corpus luteum would have degenerated within 2 weeks after its formation

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6
Q

What is the function of human chorionic gonadotropin in pregnancy?

A

1) The persistence of the corpus luteum
2) It gets into the maternal circulation and the detection of this hormone in the
mother’s plasma/urine is used as a test for pregnancy
3) stimulates the corpus luteum’s secretion of
oestrogen & progesterone (ovary)

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7
Q

what produces hCG? when?

A

Produced by the trophoblast cells around the time they begin their
endometrial invasion at day 7-8 (onset of implantation)

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8
Q

Describe the course of action of hCG in pregnancy?

A

1) hCG secreted into the maternal blood from the developing trophoblasts
2) stimulates the MATERNAL OVARIES to continue to secrete oestrogen & progesterone
3) this via negative feedback on maternal gonadotropin
4) secretion prevents additional menstrual cycles that would otherwise reuse in the loss of the implanted embryo

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9
Q

when does hCG reach peak and when does it decrease?

A
  • reaches a peak around 60 to 80 days after the last
    menstruation
  • rapidly decreases so that by the end of the third month it has reached a low concentration that remains constant till the end of pregnancy
  • Diminishes once placenta mature enough to take
    over oestrogen/progesterone production
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10
Q

Why is there a sharp increase in oestrogen and progestrone levels during last 6 months of pregnancy?

A

due to their secretion by the TROPHOBLAST CELL OF THE

PLACENTA and the corpus luteum regresses after 3 months

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11
Q

The placenta has the enzymes required for the synthesis of progesterone
but NOT those required for the formation of androgens which are the precursors of OESTROGEN.
TRUE OR FALSE???

A

TRUE

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12
Q

The placenta is supplied with androgens via:

A

1) Maternal ovaries
2) Maternal adrenal medulla
3) FOETAL adrenal medulla

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13
Q

what enzyme converts the androgens into oestrogen?

A

AROMATASE

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14
Q

Why do you get no menstrual cycles during pregnancy?

A

1) Both oestrogen & progesterone are secreted in high concentrations by the CORPUS LUTEUM and then by the PLACENTA throughout pregnancy so the secretion of the anterior pituitary gland gonadotropins remains EXTREMELY LOW
2) The secretion of GnRH and thus LH & FSH is POWERFULLY INHIBITED by high concentrations of progesterone once in the PRESENCE of oestrogen

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15
Q

PROLACTIN

  • when does it increase/ decrease?
  • where is it produced?
  • what is its function during pregnancy?
  • release controlled by?
A

1) Increases at the end of pregnancy when oestrogen & progesterone DECREASE
After birth oestrogen & progesterone levels drop DRAMATICALLY - this allows prolactin to stimulate the production of milk
2) Produced by the anterior pituitary gland
3) Has roles in milk production and the prevention of ovulation
4) Release is also controlled by suckling

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16
Q

RELAXIN

  • when does it increase/decrease?
  • where produced?
  • function?
A

1) High in early pregnancy
2) Prodcued by the ovary & placenta
3) Helps to limit uterine activity, soften the cervix and involved in cervical ripening

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17
Q

OXYTOCIN

  • when does it increase/decrease?
  • where produced?
  • function?
A
  • Secreted throughout pregnancy but increases at the end
  • Produced by the posterior pituitary gland
  • Stimulates uterine contractions during pregnancy & labour
  • Triggers caring reproductive behaviours
  • Drug used to induce labour
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18
Q

Prostaglandins

  • what are the different types?
  • where produced?
  • function?
A
  • PGF2alpha is the main one but PGE2 is 10 times more powerful
  • Produced by uterine tissues
  • Initiates LABOUR
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19
Q

Maternal physiological adaptation

What are the cardiovascular changes that happen?

A

1) Increased Cardiac Output
2) Reduced Blood Pressure
3) Reduced Total Peripheral Resistance
4) Increased Uterine Blood Flow
5) Increased Blood Volume
6) Increased Plasma & Blood cell mass

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20
Q

Why does blood pressure decrease in pregnancy?

A

There is mass vasodilation which reduces the Total peripheral resistance and so BP decreases.
BP= TRP X CO

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21
Q

Why does uterine blood flow increase in pregnancy?

A

to ensure nutrients are delivered to the foetus

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22
Q

What are the respiratory changes that happen in pregnancy?

A

Increased Alveolar Ventilation

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23
Q

what are the gastrointestinal changes in pregnancy?

A

1) Increased Acid reflux

2) Gastroparesis (delayed emptying)

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24
Q

What are the skin changes in pregnancy?

A

1) Linea nigra - dark central line on abdomen
2) Striae gravidarum - stretch marks in lumbar/lower
abdominal regions
3) Darkened areolar of breasts

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25
Q

What are the biochemical changes in pregnancy?

A

1) Weight gain - maternal & fetoplacental:
• Obese women do not put on much weight during pregnancy since they have fat stores which can be mobilised to supply the energy for pregnancy
• Skinny women do not have these fat stores so must put on weight thus they put on more extra weight during pregnancy

2) Increased Protein & Lipid synthesis
3) Insulin RESISTANCE

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26
Q

Why is there insulin resistance in pregnancy?

A
  • The hormones estrogen, cortisol, and human placental lactogen can block insulin.
  • Glucose can’t go into the body’s cells. The glucose stays in the blood and makes the blood sugar levels go up
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27
Q

What happens to veins in pregnant women? why?

A

VARICOSE VEINS.

1) increased progestin levels can dilate or open the veins.
2) the uterus puts pressure on the inferior vena cava

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28
Q

Why do pregnant women experience lumbar lordosis? what is it?

A

1) gravitational push causes the lumbar spine to become anteriorly convex
2) to compensate for the increased weight as the fetus grows

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29
Q

What is the main organ for gas exchange in the fetus?

A

the placenta

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30
Q

what do the umbilical veins carry?

A

The umbilical vein carries oxygenated, nutrient-rich blood from the placenta to the fetus

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31
Q

what do the umbilical arteries carry?

A

The umbilical arteries carry deoxygenated, nutrient-depleted blood from the fetus to the placenta

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32
Q

why is in-uterine circulation of the baby different to the outside?

A

While the baby is still in the uterus, his or her lungs are not being used. The baby’s liver is not fully developed. Circulating blood bypasses the lungs and liver by flowing in different pathways and through special openings called shunts

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33
Q

describe the blood circulation from the mother’s system to the foetus’ heart?

A

1) Oxygen and nutrients from the mother’s blood are transferred across the placenta to the fetus through the umbilical cord.
2) blood flows through the umbilical vein toward the baby’s liver. There it moves through a shunt called the ductus venosus.
3) some of the blood to go to the liver but most of it flows to the inferior vena cava and then into the right atrium of the heart.

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34
Q

What happens when the blood reaches the foetal heart?

A

1) Oxygenated blood from the mother enters into the right atrium.
2) Most of the blood flows across to the left atrium through a shunt called the foramen ovale.
3) From the left atrium, blood moves down into the left ventricle then the ascending aorta
4) From the aorta, the oxygen-rich blood is sent to the brain and to the heart muscle itself. Blood is also sent to the lower body.

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35
Q

what happens to the deoxygenated blood from the foetal body?

A

1) Blood returning to the heart from the fetal body contains carbon dioxide and waste products as it enters the right atrium.
2) It flows down into the right ventricle (normally would be sent to the lungs to be oxygenated)
3) It bypasses the lungs and flows through the ductus arteriosus into the descending aorta, which connects to the umbilical arteries.
4) Blood flows back into the placenta. There the carbon dioxide and waste products are released into the mother’s circulatory system.
5) Oxygen and nutrients from the mother’s blood are transferred across the placenta. Then the cycle starts again.

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36
Q

Role of ductus venosus

A

shunts a portion of umbilical vein blood flow directly to the inferior vena cava. It allows oxygenated blood from the placenta to bypass the liver.

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37
Q

Role of Foramen Ovale. The remnant of this can be seen as?

A

Small hole located in the septum, which is the wall between the two upper chambers of the heart (atria). Allows the baby to bypass the lungs.
FOSSA OVALIS is the remnant

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38
Q

role of ductus arteriosus

A

Is a blood vessel in the developing fetus connecting the trunk of the pulmonary artery to the proximal descending aorta.
It allows most of the blood from the right ventricle to bypass the fetus’s fluid-filled non-functioning lungs.

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39
Q

How can you tell if a lady is pregnant?

A

1) Conception/ missed period
2) Demonstrable fetal heart on ultrasound 5-6 wks
3) “Quickening” (when baby moves around 20 weeks)
4) Symphysio-fundal height (measure height of uterine fundus)
5) Head engagement
6) Show (blood stained vaginal discharge just before labour)
7) Labour

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40
Q

cephalic position

A

when foetus head is at the bottom, near the neck of womb. How it should be normally

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41
Q

breech presentation

A

a baby is orientated with another part of the body downwards

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42
Q

Should the height of the fundus correspond to the progression of the pregnancy?

A

The height of fundus should correspond to the progression of the pregnancy.

But we know that the size of the baby is also corresponding to the size of the mother, age of the mother,race of mother and no of kids before so we have customised charts for the fundal height.

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43
Q

Common maternal problems affecting pregnancy

A

1) Biological factors
- Poor weight gain/undernutrition
- Extremes of maternal age
2) Medical conditions
3) Drug misuse: cigarettes, heroin etc
4) Haemorrhage

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44
Q

Common fetal problems affecting pregnancy

A

1) Miscarriage
2) Abnormal development
3) Disordered fetal growth
- Too big
- Too small
4) Premature birth and consequences

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45
Q

Breast changes in pregnancy

A

1) increase in size and shape
2) nipples increase in size and become more erect
3) areola become larger and more darkly pigmented
4) Montgomery’s tubercles become more active and secrete substances that lubricates the nipples

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46
Q

How long does normal pregnancy last?

A

Normal pregnancy lasts around 40 weeks. Counting from the first day of the last
menstrual cycle OR around 38 weeks - counting from the day of ovulation and
conception

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47
Q

Define Parturition

A
  • Is the birth process
  • events that occur in the uterus & foetus in the last few weeks of pregnancy that culminate in delivery)
  • Resulting in the successful transition from intra-uterine to extra-uterine life
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48
Q

Throughout most of pregnancy the smooth muscle cells of the myometrium are?
what is this maintained by?

A

The smooth muscle cells of the myometrium are

relatively disconnected from each other. This feature is maintained mainly by progesterone.

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49
Q

what happens in the last few weeks of pregnancy to the smooth muscle cells of the myometrium?

what causes this?

A

1) During the last few weeks of pregnancy the smooth muscle cells synthesis CONNEXINS
2) These are proteins that form gap junctions between the cells, which allow the myometrium to undergo coordinated contractions

3)This is as a result of the increasing concentrations of oestrogen

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50
Q

What is cervical ripening

A

growth & remodelling of the cervix prior to labour

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51
Q

When and what accelerates the process of cervical ripening?

A

1) Process is accelerated during the last 3 months of pregnancy due to the presence of oestrogen
2) During pregnancy the uterus is sealed at its outlet by the firm, inflexible collagen fibers
3) This feature is maintained mainly by progesterone
4) In the last few weeks of pregnancy, at the same time that the connexins are forming, the cervix becomes soft & flexible due to an enzymatically mediated breakdown of its collagen fibres

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52
Q

what mediates the synthesis of the enzymes needed for cervical ripening?

what do they do?

A

1) Oestrogen
2) Placental prostaglandins - PGE
3) Relaxin:
- Secreted by the ovaries, placenta & uterus
- It softens cartilaginous joints in the pelvis in preparation for labour

  • Causes the effacement and dilation due to muscular action of cervix and uterus.
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53
Q

firmness of the cervix before/after?

A

Before pregnancy the cervix is as firm as the tip of your nose, by the end of pregnancy the cervix is as firm as your lips.

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54
Q

what happens to oestrogen, progesterone and prostaglandin levels during labour?

A
  • more oestrogen
  • less progesterone
  • more prostaglandin
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55
Q

what are three phases of parturition? what happens in each?

A

1) Myometrial repression
No contraction of uterus
2) Myometrial activation
The uterus can begin to get ready contract
Due to increasing oestrogen levels
3) Biochemical changes/ permanent change
When the contraction can begin
Due to high levels of prostaglandins

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56
Q

Where are Prostaglandins (PG) synthesised?
Which ones are the main ones?
Which one is mainly released in labour?

A
  • All uterine tissues able to synthesize PG
  • Mainly E2 and F2alpha
  • PGE2 is about 10 times as potent as PGF2a in the human uterus.
  • PGF2a - main prostaglandin released during labour
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57
Q

What happens in pre-labour?

maternal and foetal signs?

A

The initiation of labour:
Maternal signal : oxytocin
Foetal signal: oxytocin, vasopressin & cytokines1)

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58
Q

Pre-labour what happens?

A

1) myometrium smooth muscle cells are capable of autonomous contractions
2) facilitated as the muscle is stretched by the growing foetus
3) Near term, prostaglandins are released from the decidua and chorioamnion
4) these prostaglandins (esp PGF2alpha) are potent stimulators of contractions and also enhance the action of oxytocin
5) Oxytocin is released from posterior pituitary
6) these act on smooth muscle to contract

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59
Q

What triggers the release of oxytocin?

what does it do?

A

1) Neural input from the receptor cells in the uterus. the number of these receptors increases in last few weeks
2) they act on uterine smooth muscle
3) they synthesise prostaglandins

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60
Q

describe the positive feedback mechanism of labour contractions

A

1) the fetus’ head pushes downward
2) this stretches the cervix
3) this causes the hypothalamus to increase the action potential frequency from the oxytocin neuron cell bodies
4) this causes increases oxytocin secretion from the posterior pituitary
5) so the plasma oxytocin increases
6) so uterus contractions increase
7) causing the cervix to stretch even more and even more signals from stretch receptors go to the hypothalamus

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61
Q

role of prostaglandins in labour

A

1) Initiated by increased PGFa
2) enhances the action of oxytocin
3) resulting in myometrial contraction
4) which in turn exert pressure on the cervix and promotes further contraction

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62
Q

What happens at the onset of labour?

A

the amniotic sac RUPTURES and the amniotic fluid flows through the vagina

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63
Q

Describe the nature of contractions in labour

What is the maximum diameter of the cervix?

A

1) When labour begins in earnest the uterine contractions become stronger and occur at approximately 10 to 15 minute intervals
2) The contractions begin in the upper portion of the uterus and sweep downwards
3) As the contractions increase in intensity and frequency, the cervix is gradually forced open (dilation) to a maximum diameter of around 10cm

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64
Q

What are the 3 components of labour?

A

1) the passenger -the baby
2) the passage -the pelvis
3) the power- the uterus

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65
Q

what is special about the fetal skull?

A
  • The sutures in the skull of the baby are not fully fused together
  • They have gaps like the diamond shaped anterior fontanelle and triangular posterior fontanelle
  • This allows for the collapse of the skull to allow it to come out of the uterus.
  • These bones can override.
  • You can use these frontalles to see the position of the baby.
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66
Q

the passage- the pelvis

A

The WIDER THE pelvis, there is more space for the baby to come out.

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67
Q

the power - the uterus

A

1) Influx of Ca in myometrium, these interact with calmodulin.
2) This causes the phosphorylation of MLCK
3) This leads to interactions between myosin and actin in the myometrium

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68
Q

What are Braxton-Hicks contractions?

A
  • These are painless contractions of the myometrium
  • Not coordinated
  • By the end of pregnancy they have more heavy contractions, which are in more of a coordinated fashion
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69
Q

Role of Adrenocorticotropic hormone (ACTH) in labour

A

1) The fetus anterior pituitary gland releases more ACTH
2) this causes the adrenal gland to release more glucocorticoids and androgens
3) this increases the oestrogen in the placenta
4) so more prostaglandins

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70
Q

3 phases of labour

A

1) LATENT PHASE (6hr-3days)

2) ACTIVE PHASE ( 3 MORE STAGES)
1ST STAGE - 10mm
2ND STAGE - DELIVERY
3RD STAGE - DELIVERY OF PLACENTA

3) POSTPARTUM PHASE

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71
Q

what problems can occur with passages?

A

Too narrow
Too wide
Damaged

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72
Q

what problems can occur with passenger?

A

Too large or too small
Abnormal lie or presentation eg breech
Tumours
Too poorly

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73
Q

what problems can occur with powers?

A
  • Too strong (not enough time of placenta to relax and fill up with oxygen so baby will get hypoxic
  • Too weak
  • Disorganised contractions
  • Cervix too rigid
  • Cervix weak
  • Postpartum bleeding
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74
Q

problems with the stages of labour

A
  • Prolonged latent phase
  • Failure to progress in labour
  • Delayed 2nd stage – instrumental delivery
  • Delayed 3rd stage – manual removal of the placenta
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75
Q

what provides the nutrients for the embryo in the first few weeks?
what takes over?

A
  • The simple nutritive system from the endometrial cells is only adequate to provide for the embryo during the FIRST FEW WEEKS when the embryo is very
    small
  • The structure that takes over this function is
    the PLACENTA
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76
Q

what is the embryonic portion of the placenta supplied by?

A

is supplied by the outermost layers of
trophoblast cells, the
VILLUS CHORION:

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77
Q

what is the maternal portion supplied by?

A

Decidua Basalis, the uterine lining forming the

maternal part of the placenta, underlying the chorion

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78
Q

what is the first stage of placental development?

A

blastocyte IMPLANTATION

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79
Q

development of the placenta

A

1) The 8 cell MORULA arrives in the uterus and develops into the blastocyst
2) The outer cell layer from the primary trophoblastic cell mass (TCM)
3) TCM then invades the endometrium which degenerates and the trophoblast contacts stroma
4) Implantation is complete by the 11th day POST OVULATION

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80
Q

what are the chorionic villi?

A

Finger-like projections of the trophoblast cells that extend from the chorion into the endometrium

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81
Q

what is the role of the chorionic villi?

A

1) The villi contain a rich network of capillaries that are part of the embryo’s
circulatory system
2) The endometrium around the villi is altered by enzymes & other paraffin
molecules secreted from the cells of the invading villi so that each villus
becomes completely surrounded by a pool or placental sinus of maternal
blood

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82
Q

How does the maternal blood enter and exit the placental sinuses?

A
  • The maternal blood enters these placental sinuses via the UTERINE
    ARTERY
  • The blood flows through the sinuses
  • Then exits via the UTERINE VEINS
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83
Q

how does the blood flow from the foetus into the capillaries of the chorionic villi?

A

via the umbilical ARTERIES

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84
Q

how does the blood move out of the capillaries back to the foetus?

A

via the Umbilical VEIN

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85
Q

What contains all of the umbilical vessel?

A

All of these umbilical vessels are contained in the umbilical cord (rope-like structure that connects the foetus to the placenta).

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86
Q

What does the placenta provide for the foetus?

A
  • Nutrition
  • gas exchange
  • waste removal
  • endocrine and immune support
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87
Q

3 main functions of the placenta

A

metabolism, transport and endocrine

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88
Q

Placental Metabolism

A

1) Synthesises:
- Glycogen
- Cholesterol
- Fatty acids

2)Provides nutrients & energy

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89
Q

Placental Transport

what does it transport (11 things)? how?

A

Transports:

1) Gases & nutrition; O2 & CO2 - to & from baby, CO
2) Water
3) Glucose (facilitated diffusion via hexose transporters)
4) Vitamins
5) Amino acids - by active transport
6) Hormones, mainly steroid NOT PROTEIN
7) Electrolytes
8) Maternal antibodies IgG and NOT IgM
9) Waste products; urea, uric acid & bilirubin
10) Drugs and their metabolites
11) Infectious agents

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90
Q

What type of bilirubin is easily transported?

A

Un-conjugated from foetus crosses placenta easily

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91
Q

how can fetal drug addiction be caused?

A

Drugs and their metabolites are transported to the baby via the placenta so they also become dependant on it

92
Q

Placental barriers to transport (from maternal to foetus)

A

1) Maternal endothelial cells
2) Maternal connective tissue
3) Endometrial epithelial cells
4) Chorionic epithelial cells
5) Fetal connective tissue
6) Fetal endothelial cells

93
Q

when does the heart begin to pump and placenta is well established?

A

Five weeks after implantation

94
Q

where is the amniotic cavity?

A

A space forms between the inner cell mass and the chorion whilst the placenta develops

95
Q

What is the amniotic sac?

A

The epithelial layer lining the amniotic cavity is derived from the inner cell mass

96
Q

What is the role of the AMNIOTIC FLUID?

A

1) AMNIOTIC FLUID resembled the fetal extracellular fluid
2) It buffers mechanical disturbances and temperature
variations
3) The foetus floats in the amniotic cavity and is attached by the umbilical cord to the placenta

97
Q

What is placenta accreta?

A

abnormal adherence, with absence of decidua basalis

98
Q

What is placenta percreta?

A

villi penetrate myometrium

99
Q

What is placenta praevia?

A
  • placenta overlies internal of uterus
  • abnormal bleeding
  • usually requires cesarean delivery
100
Q

What are Cord abnormalities?

A
  • knotting 1%, prevents the passage of placental blood

* Single umbilical artery

101
Q

What type of glands are endocrine glands and what do they do?

A

Endocrine glands are ductless and release hormones directly into blood

102
Q

What is the purpose of the endocrine system?

A

Main purpose of the endocrine system is to release hormones directly into the blood. This inturn:
• Allows for rapid adaptive changes
• integration of whole body physiology
• chronicmaintenance of metabolic environment
• the communication for multi-cellular organisms

103
Q

What is a hormone?

A

A hormone is a substance secreted directly into the
blood by specialised cells.
Hormones are present in only minute concentrations in the blood and bind specific receptors in target cells to influence cellular reactions.

104
Q

Name some common hormones

A
  • Insulin
  • Cortisol
  • Testosterone
  • Thyroxine
  • Adrenaline
105
Q

Name the endocrine glands

A

1) Hypothalamus
2) Pituitary
3) Thyroid
4) Parathyroid
5) Adrenals
6) Pancreas
7) Ovaries/Testes

106
Q

Some organs can also act as endocrine organs. How does Fat tissues do this?

A

They convert fat into active androgens

107
Q

What are the different types of hormones?

give example

A

STEROID

  • All steroid hormones are derived from cholesterol.
    e. g. Glucocorticoids

PEPTIDE
e.g. ANP

THYROID
e.g. thyoroxine

108
Q

What is the half life of a hormone?

A

A hormone’s half-life is the time required for half the concentration of the hormone to be degraded.

109
Q

What do G proteins coupling receptors do?

A

Also called seven-transmembrane receptor is a protein located in the cell membrane that binds extracellular substances and transmits signals from these substances to an intracellular molecule called a G protein. The G protein then activates a cascade of reaction.

110
Q

How do we measure hormone levels?

A

1) Bioassays
2) Immunoassays
3) Mass spectrometry

111
Q

What are the main Anterior pituitary hormones?

and their functions?

A 
1) ACTH
Regulation of adrenal cortex
2)TSH
Thyroid hormone regulation
3) Growth Hormone 
Growth (+), metabolism
4) LH/FSH
Reproductive control
5) Prolactin
Breast milk production
112
Q

what are the main Posterior pituitary hormones?

A

1) ADH
water regulation
2) Oxytocin
breast milk production

113
Q

Thyrotoxicosis

A
  • too much thyroid

- caused due to antibodies against your thyroid hormone receptors so TSH is supressed

114
Q

Cushing’s disease

A
  • too much cortisol due to too much ACTH
115
Q

Acromegaly

A
  • too much growth hormone
116
Q

Where is the thyroid gland located?

A
  • Endocrine structure located in the neck
  • Located in the anterior neck between C5-
    T1 vertebrae
  • Lies behind the sternohyoid & sternothryoid muscles
  • Wraps around the cricoid cartilage and superior tracheal rings
  • Lies inferior to the thyroid cartilage of the larynx
117
Q

What are the two lobes of the thyroid gland connected by?

A

isthmus

118
Q

Why is the thyroid gland high vascularised?

A

It secretes hormones directly into the blood

119
Q

What supplies the blood to the thyroid gland?

A

Achieved by two main arteries: superior and inferior thyroid arteries.

120
Q

Superior thyroid artery

  • branch of?
  • route?
  • supplies?
A

1) first branch of the extrenal carotid artery
2) after arising the artery descend towards the thyroid gland
3) supplies the superior and anterior portions of the gland

121
Q

Inferior thyroid artery

  • branch of?
  • route?
  • supplies?
A

1) arises from the thyrocervical trunk which in turn is a branch of the subclavian artery
2) artery travels
superomedially to reach the inferior of the gland
3) to supply the postern-inferior aspect

122
Q

what is the thyroid gland innervated by and what controls the hormone release?

A

Innervated by branches from the sympathetic trunk but sympathetic innervation DOES NOT control hormone release, this is controlled by the PITUITARY GLAND

123
Q

Describe the embryology of the thyroid gland

A
  • At 3-4 weeks the thyroid glands appear as an epithelial proliferation at the base of the pharynx
  • The glands then migrate down the thyroglossal duct to below the larynx
  • The glands begin producing thyroxine at 18-20 weeks
124
Q

What happens if the thyroid gland descends too far during embryology?

A

Possible sites of ectopic thyroid tissue, thyroglossal

cysts and pyramidal lobe

125
Q

Describe the histology of a follicle

A
  • Made from enclosed sphere of follicular cells surrounding a core containing a protein-rich material
    called the colloid.
  • Centre is called COLLOID and contains thyroglobulin in which iodine is STORED and taken up from the blood.
126
Q

Describe the histology of a follicular cells

A
  • SIMPLE CUBOIDAL EPITHELIUM
  • Becomes COLUMNAR with increased metabolic activity
  • Arranged into hollow spheres called follicles
  • Produce hormones T3 & T4
127
Q

C-cells

A

Produce calcitonin for Ca2+ homeostasis. Calcitonin is used as a tumour marker for tumours here.

128
Q

Where are thyroid hormone receptors present?

How does thyroid hormone work?

A

Receptors for thyroid hormone are present in the nuclei of most cells in the body, unlike receptors for many other hormones (whose distribution is more limited).
• The actions of T3 are WIDESPREAD and affect many organs and tissues
• Like steroid hormones, T3 acts by inducing gene transcription and protein synthesis

129
Q

Overall actions of thyroid hormone

A

1) Control of Basal Metabolic Rate
2) Regulation of growth
3) Brain maturation

130
Q

What are the metabolic actions of the thyroid hormone?

A

1) T3 stimulates carbohydrate absorption from the small intestine and increases fatty acid release from adipocytes
2) These actions provide energy that helps maintain METABOLISM at a HIGH RATE
3) Much of that energy is used to support activity of Na+/K+- ATPases throughout the body; these enzymes are also stimulated by T3.
4) When the activity of Na+/K+-ATPases increases (stimulated by T3) then a by-product of this is heat
5) Thus another action of T3 is to produce heat which is essential for body temperature homeostasis
6) Without thyroid hormone heat production would decrease and body temperature would be compromised

131
Q

what are the permissive actions of thyroid hormone?

what will an over-active thyroid do?

A

T3 up-regulates beta-adrenergic receptors (for adrenaline) in many tissues such as the heart & nervous system.
Thus in over-active thyroid with excess T3 the symptoms are similar to that of excess adrenaline e.g. racing heart, anxiety & nervousness

132
Q

What is the role of thyroid hormone in growth and development?

A

T3 is required for the normal production of GROWTH HORMONE from the anterior pituitary.

133
Q

What is the role of thyroid hormone in nervous system development?

A

During fetal life T3 helps in:
• Formation of axon terminals
• Production of synapses
• Growth of dendrites & dendritic extensions
• Formation of myelin
T3 is also required for proper nerve & muscle reflexes and for normal cognition in adults.

134
Q

Describe the control of thyroid function

A

1) Neural inputs causes the hypothalamus to secrete thyroid-releasing hormone (TRH)
2) This stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH)
3) This causes the thyroid gland follicular epithelial cells to produce and secrete more T3 and T4 so the plasma thyroid hormone concentration increases
4) At target cells the T4 is converted to T3.

135
Q

What is the negative feedback mechanism in terms of the thyroid gland?

A

The basic control mechanism of TSH production
is the negative feedback action T3 & T4 on the
anterior pituitary gland and to a lesser extent,
the hypothalamus

136
Q

What are the actions of TSH on the thyroid gland?

A

1) stimulates production of T3 and T4
2) increases PROTEIN SYNTHESIS in follicular cells
3) increases DNA replication & cell division
4) increases the amount of rough endoplasmic reticulum and other cellular machinery required by follicular cells for protein synthesis

137
Q

What would happen is the thyroid glands were exposed to too much TSH?

A

The cells will undergo hypertrophy - they will increase in size (an enlarged thyroid gland from any
cause is called goiter)

138
Q

What is thyroxine?

A
  • Hormone produced by the thyroid gland
  • T4 since it contains 4 iodines
  • CH2CH(NH2)COOH
  • most abundant but reservoir for additional T3
139
Q

What is TRIIODOTHYRONINE?

A
  • Hormone produced by the thyroid gland
  • T3 since it contains 3 iodines
  • CH2CH(NH2)COOH
  • major active form
140
Q

How is t4 converted to t3?

A

T4 is generally converted into T3 by enzymes known as deiodinases in target cells.

141
Q

Describe the process of T1 and T2 synthesis . All steps

A

1) TSH binds to TSH receptor which is a g-coupling receptor
2) TSH stimulates circulating IODIDE to be actively cotransported with Na+ ions across the basolateral membranes of the follicular cells - this is known as
IODIDE TRAPPING, the Na+ is pumped back out of the cells via Na+/K+- ATPases
3) The negatively charged iodide ions then diffuse to the apical membrane of the follicular cells and are transported into the colloid
4) The colloid of the follicles contains large amounts of a protein called THYROGLOBULIN
5) Once inside the colloid the iodide is rapidly oxidised to IODINE which then bind to TYROSINE RESIDUES on the thyroglobulin molecules under the action of the enzyme thyroid peroxidase
6) The tyrosine may either bind to ONE IODINE MOLECULES - in which case its
called a monoiodotyrosine (T1)
7) The tyrosine may bind to TWO IODINE MOLECULES - in which case its called a diiodotyrosine (T2)

142
Q

What happens to the T1 and T2 when the thyroid is stimulated to produce thyroid hormone? How is T3 and T4 made?

A

When the thyroid is STIMULATED to produce thyroid hormone, the T1 and T2 molecules are cleaved from their tyrosine backbone (but are still attached to
the thyroglobulin) and join to create T3 (T1 + T2) or T4 (T2 + T2)

143
Q

How does the T3 and T4 get released into blood stream?

A

1) Extensions of the colloid- facing membranes of the follicular cells engulf portions of the colloid (with its iodinated thyroglobulin) by endocytosis
3) The iodated thyroglobulin is then brought into contact with lysosomes in the cell interior
4) PROTEOLYSIS of the thyroglobulin results in the release of T3 & T4 which then are able to diffuse out of the follicular cells into the interstitial fluid and
from there into the blood

144
Q

What happens if you are short of dietary iodine?

A

There is sufficient iodinated thyroglobulin stored within follicles of the thyroid to provide thyroid hormone for several weeks even in the absence of dietary iodine - this is unique amongst endocrine glands.

145
Q

What are some thyroid hormone binding proteins?

Conc of FREE T3 and T4?

A

1) TBG, Albumin, Transthyretin
2) Free T3= 0.3%
Free T4= 0.03%

146
Q

What do we look at in thyroid function tests?

A

1) Serum TSH
2) Serum FREE T4
3) Serum FREE T3

147
Q

What does the test profile look in HYPERthyroidism? WHY?

A
  • LOWER TSH
  • INCREASED free T3
  • INCREASED free T4
    negative feedback
148
Q

What does the test profile look in HYPOthyroidism? WHY?

A
  • INCREASED TSH
  • DECREASED free T3
  • DECREASED free T4
    to stimulate more thyroid hormone
149
Q

Is hyper/hypothyrodism more common in male or females?

A

FEMALES

150
Q

What is the aetiology of hyperthyroidism?

A
  • Graves’ hyperthyroidism (auto-antibodies stimulating the TSH receptor)
  • Toxic nodular goitre (single or multinodular)
  • Thyroiditis- inflammation
  • Exogenous iodine
  • Factitious (taking excess thyroid hormone)
  • TSH secreting pituitary adenoma
  • Neonatal hyperthyroidism
151
Q

What is the aetiology of hypothyroidism?

A

MORE COMMON

  • Autoimmune: Hashimoto’s thyroiditis
  • After treatment for hyperthyroidism
  • Subacute/silent thyroiditis
  • Iodine deficiency
  • Congenital (thyroid agenesis/enzyme defects)
152
Q

Name some signs and symptoms of hyperthyroidism?

  • cardiovascular
  • neurological
  • gastrointestinal
  • eyes/skin
A 
Cardiovascular
- Tachycardia (rapid heart rate)
- AF (atrial fibrillation)
- Shortness of breath
- Ankle swelling
Neurological 
- Tremor
- Myopathy (muscle weakness)
- Anxiety
Gastrointestinal 
- Weight loss
- Diarrhoea
- Increased appetite
Eyes/skin 
- Sore, gritty eyes
- Double vision
- Staring eyes
- Pruritus (itching)
153
Q

Name some signs and symptoms of hypothyroidism?

  • cardiovascular
  • neurological
  • gastrointestinal
  • eyes/skin
A 
Cardio
- Bradycardia (slow heart rate)
- Heart failure 
Gastrointestinal 
- weight gain 
- constipation 
Skin 
- Myxoedema 
- vitiligo 
Neurological 
- depression 
- psychosis
154
Q

Parathyroid gland anatomy

A
  • 4 glands behind thyroid
  • close proximity to Recurrent Laryngeal Nerve
  • No direct blood supply
155
Q

Function of parathyroid gland

A
  • Regulate calcium and phosphate levels
  • Release PTH in response to: low calcium or high phosphate
  • Binds to G protein coupled receptors mainly in
    kidney and osteoblasts
  • check MSK for actions of PTH
156
Q

What inhibits PTH transcription?

A 
PTH transcription (mRNA production) is inhibited by
1,25D3.
157
Q

What inhibits PTH translation?

A

PTH translation (mRNA to protein synthesis) is inhibited by increased serum calcium.

158
Q

Where is calcitonin produced? What does it do?

A

Produced by thyroid c-cells (parafollicular). Calcitonin released in hypercalcaemia,
inhibits bone resorption (by direct effect on osteoclasts)

159
Q

Primary hyperparathyroidism

cause, blood profile, treatment

A

– parathyroid tumour (usually benign adenoma)
– Causes hypercalcaemia and low serum phosphate
– Loss of negative feedback from hypercalcaemia
– (Treatment is surgery)

160
Q

Secondary hyperparathyroidism

cause, blood profile, treatment

A

– renal disease (increased phosphate, decreased activation of vitamin D)
– (Treatment with phosphate binders or vitamin D analogues)

161
Q

Tertiary hyperparathyroidism

cause, blood profile, treatment

A

– long-standing secondary HPT leads to irreversible parathyroid hyperplasia.
Usually seen when renal disease corrected e.g. by transplantation
– (Treatment is surgery)

162
Q

Mitosis summary

A
  • Produces 2 genetically identical daughter cells

- occurs in embryonic growth and tissue repair

163
Q

Meiosis summary

A
  • produces haploid gametes
  • meiosis 1: separates homologous chromosome pairs producing 2 haploid cells
  • meiosis 2: separates duplicated sister chromatids producing 4 haploid
164
Q

Genotype

A

The complete genetic composition of an individual is known as the genotype

165
Q

Male sex chromosome

Female sex chromosome

A
  • Males = XY

- Females = XX

166
Q

Why is it that the male determines the fetal sex?

A

The ovum can only contribute an X chromosome, whereas half of the
sperm produced during meiosis are X & half are Y.

167
Q

Lyonisation

A

When two X chromosomes are present (in a female), only one is functional, the non-functional X chromosome condenses to form a nuclear mass called
the sex chromatin or BARR BODY.

The single X chromosome in males rarely condenses to form sex chromatin.

168
Q

Where are do male and female gonads derive from embryologically?

A

The urogenital ridge

169
Q

Until when are the primordial gonads undifferentiated?

A

Up until the 6th week of uterine life, primordial gonads are undifferentiated

170
Q

Before the functioning of the fetal gonads, What does the undifferentiated reproductive
tract include?

A

A double genital duct system comprised of the:

  • Wolffian ducts
  • Mullerian ducts
  • Common opening to the outside for the genital ducts & urinary system
171
Q

Describe the process of sex development in males.

A

1) There is migration of the primordial germ cells from the dorsal endoderm to the urogenital ridge by 6-8 weeks.
2) The primordial gonads are undifferentiated
3) Males have XY sex chromosome. During the 7th week the testes start to develop. This is due to the expression of the SRY gene of the sex determining region of the Y chromosome in the urogential ridge cells.
4) The sertoli cells of the testes produce MULLERIAN-INHIBITING FACTOR (MIF)
5) This leads to the regression of the Mullerian tubes
6) The leydig cells of the testes produce TESTOSTERONE
7) This causes the wolffian duct to differentiate into epididymis, vas deferens, seminal vesicles and ejaculatory duct.

172
Q

Explain how the external genitalia form in males

A

1) The testosterone is converted to DIHYDROTESTOSTERONE by the 5alpha- reductase 2 enzyme.
2) They have a common genital tubercle at 8 weeks, with lateral urethral folds, labioscrotal swellings
3) Tubercle becomes glans penis
4) The urethral folds become corpus spongiosum enclosing urethra
5) Labioscrotal folds fuse to form scrotum and ventral penis

6) This all causes the development of the:
- Penis
- Scrotum
- Prostate

173
Q

Describe the process of sex differentiation in females

A

1) There is migration of the primordial germ cells from the dorsal endoderm to the urogenital ridge by 6-8 weeks
2) The primordial gonads are undifferentiated
3) Due to the absence of the Y chromosome, and therefore no SRY gene expressed, testes do not develop, instead ovaries begin to develop in the same area.
4) There is no testes so NO TESTOSTERONE OR MIF
This means that the Mullerian ducts do not regress and develop into
- Fallopian tubes
- Uterus
- Inner vagina

5) The Wolffian ducts regress as no testosterone

174
Q

Explain the formation of external genitalia in females

A

1) Due to the absence of testosterone there is the development of the outer vagina and the female external genitalia
2) They have a common tubercule at 8 weeks, with lateral urethral folds, labioscrotal swellings
3) Tubercle becomes clitoris
4) Urethral folds become labia minora
5) Labioscrotal folds fuse to form labia majora

175
Q

Germ cells

A
  • Cells that develop into sperm & ova
  • Originate from the yolk sac of the hind gut
  • Specialised cells which develop into gametes
176
Q

Other name for wolffian ducts

A

Mesonephric duct

177
Q

Other name for mullerian ducts

A

Paramesonephric duct

178
Q

Describe the first stage of gametogenesis

- timings in males and females

A

The first stage is proliferation of the primordial (undifferentiated) germ cells by MITOSIS.

The timing of mitosis in germ cells differs greatly in females & males:
• In males, some mitosis occurs in the embryonic testes to generate the population of PRIMARY SPERMATOCYTES present at birth, but mitosis
really begins during male puberty and usually continues throughout life

• In females, mitosis of germ cells in the ovary occurs primarily during fetal development resulting in the generation of PRIMARY OOCYTES.

179
Q

Describe the second stage of gametogenesis

A

The second stage of gametogenesis is MEIOSIS resulting in the gametes receiving only 23-chromosomes from a 46 chromosome germ cell - one
chromosome from each homologous pair.

The results of the FIRST MEIOTIC DIVISIONS are:
• Secondary spermatocytes (2) in males
• Secondary oocyte (1) in females

The SECOND MEIOTIC DIVISION:
• The timing of the second meiotic division is different in males & females:
- In males this occurs continuously AFTER puberty with the production of spermatids and ultimately mature sperm cells
- In females the second meiotic division does not occur until AFTER FERTILISATION of a secondary oocyte by a sperm - this results in the production of a zygote (contains 46 chromosomes - 23 from the oocyte (maternal) & 23 from the sperm (paternal)) & the second polar body which also has no function

180
Q

What is a polar body?

A

In females the second cell arising from the first meiotic division is the first polar body which has no function.

181
Q

Describe the process of mitosis in gametogenesis

A

With the exception of gametes the DNA of each nucleated human cell is contained in 23 pairs of chromosome giving a total of 46. The two corresponding chromosomes in each pair are said to be homologous to each other, with one coming form each parent
1) In mitosis the 46 chromosomes of the dividing cell are replicated
2) The cell then divides into two new cells called daughter cells
3) Each of the two daughter cells resulting from the division receive a full set of 46 chromosomes that are IDENTICAL to those of the original cell - thus the
daughter cell receives identical genetic information during mitosis.

182
Q

Describe the first meiotic division in gametogenesis

A

1) During interphase (which precedes a mitotic division) chromosomal DNA is replicated. An interphase cell has 46 chromosomes, but each chromosome consists of two identical strands of DNA, called sister chromatids which are joined together by a centromere.

2) As the first meiotic division begins, homologus chromosome, each consisting of two identical sister chromatids, come together and line up
adjacent to each other - thus 23 pairs of homologous chromosomes (sometimes called bivalents) are formed

3) The sister chromatid of each chromosome condense into thick, rodlike structures

4) Then within each homologous pair, corresponding segments of homologous chromosomes align closely
This allows two non-sister chromatids to undergo an exchange of sites of breakage in a process known as crossing over. Crossing over results in the recombination of genes on homologous chromosomes. RECOMBINATION creates genetic diversity

5) After crossing-over the homologous chromosomes line up in the centre of the cell. The orientation of each pair on the equator is RANDOM

6) The cells then DIVIDES with the maternal
chromatids of any particular pair going to one of the two cells, resulting from the division and the paternal chromatids going to the other.

183
Q

Describe the second meiotic division in gametogenesis

A

Occurs without any further replication of DNA
• The sister chromatids of each chromosome separate and move apart into the new daughter cells
• The daughter cells arising from the second meiotic division thus contain 23 one-chromatid chromosomes

184
Q

What is TUNICA ALBUGINEA?

A

TUNICA ALBUGINEA - white fibrous
capsule:
- Septa divides the organ into compartments containing seminiferous tubules where sperm are produced.

185
Q

Why is it important that during gestation the testes descends from the abdomen to the scrotum?

A

It is essential for normal sperm producing during adulthood since normal sperm function requires a temperatures approximately 2 degrees LOWER than normal body temperature.

186
Q

How is the cooling mechanism achieved in the testes?

A

Cooling is achieved by air circulating around the scrotum and by a heat-exchange mechanism in the blood vessels supplying the testes - PAMPINIFORM PLEXUS

187
Q

Key points to remember about the seminiferous tubules

A
  • The site of SPERMATOGENESIS)
  • In the centre= fluid filled lumen containing mature sperm, spermatozoa
  • Tubular wall on the outer= developing germ cells and seratolli cells
  • seminiferous tubules» rete testis&raquo_space; efferent ductules» epididiymis&raquo_space;>vas deferens
188
Q

What type of epithelium does rete tetsis have?

A

simple cuboidal

epithelium

189
Q

What type of epithelium does efferent tubules have?

A

pseudostratified columnar epithelium

190
Q

What type of epithelium does epididymis have?

A

pseudo-stratified columnar epithelium with stereocilia

191
Q

What type of epithelium does Vas Deferens have?

A

pseudo-stratified columnar epithelium with stereocilia and is lined by smooth muscle

192
Q

What are the three glands that produce seminal fluid?

A

BULBOURETHRAL, PROSTATE & SEMINAL VESICLES

193
Q

What is semen?

A

The seminal fluid AND sperm cells are collectively termed SEMEN (with the sperm contributing a small percentage of the volume)

194
Q

What is the composition of semen?

A
  • 60% seminal vesicle fluid
  • 30% prostatic
  • 10% sperm & trace of bulbourethral fluid
195
Q

Normal sperm count

A

50-120million/mL

196
Q

Name some of the chemical substances that the prostatic, bulborethral and seminal vesicle secretions contain?

A

1) Buffers for protecting sperm against the ACIDIC VAGINAL SECRETIONS & residual urine in the male urethra
2) Chemicals (particularly from the seminal vesicles) that increase sperm motility e.g. fructose to provide energy for sperm motility
3) Prostaglandins - to stimulate female peristaltic contractions
4) BR glands produce small amount of lubricating mucoid

197
Q

Path of sperm to the outside.

SREEVE UP

A 
S - Seminiferous tubules
R - Rete testis
E - Efferent ducts
E - Epididymis
V - Vas Deferens
E - Ejaculatory duct

U - Urethra
P - Penile Urethra

198
Q

Blood testis barrier

A

1) Each seminiferous tubule is bounded by a basement membrane
2) Each sertoli cell extends from the basement membrane all the way to the lumen in the centre of the tubule and is joined to adjacent sertoli cells by means of TIGHT JUNCTIONS
3) Sertoli cells form an unbroken ring around the circumference of the seminiferous tubule
4) The ring of interconnected sertoli cells from the SERTOLI CELL BARRIER (blood-
testes barrier) which prevents the movement of many chemicals from the blood into the lumen of the seminiferous tubule and helps to retain luminal fluid

199
Q

Function of the blood testis barrier

A

1) Ensures proper conditions for germ cell development and differentiation within the tubules
2) The arrangement of sertoli cells also permits different stages of spermatogenesis to take place in different compartments and thus different environments

200
Q

How many days does spermatogenesis take?

A

64 days

201
Q

Describe the process of spermatogeneisis

A

1) The undifferentiated germ cells are called
spermatogonia - they begin to divide MITOTICALLY at puberty:
2) They produce 2 types of daughter cell:
• Type A: remain outside the blood-testis barrier & produce more daughter cells until death
• Type B: differentiate into PRIMARY SPERMATOCYTES
(takes place entirely in the basal compartment)
3) Primary spermatocytes must pass through the blood-testis barrier, to do this they pass through the tight junctions of the sertoli cells (which opens in front of them at the same time forming new tight
junctions behind them) to going entry into the central compartment.
4) Once in the central compartment the type B cells then undergo MEIOSIS 1 to produce 2 SECONDARY
SPERMATOCYTES
5) In MEIOSIS 2 the secondary spermatocytes differentiate into 4 SPERMATIDS
6) The spermatids then differentiate into spermatozoa
7) When sperm formation is complete, the cytoplasm of the sertoli cells around the sperm retracts and the sperm are released into the lumen to be bathed in luminal fluid

202
Q

What is spermiogenesis? Where does it take place?

A
  • The transformation from spermatids to spermatozoa (mature sperm) is called SPERMIOGENESIS.
  • It grows a tail and discards cytoplasm to become lighter.
  • It happens whilst contained in recesses formed by the
    invaginations of the Sertoli cell plasma membranes.
203
Q

How much sperm produced per second by per gram of testis?

A

300-600 sperm are made per gram of testis per second.

204
Q

Key points about Spermatozoa

A

1) Head is pear shaped
2) Nucleus with the haploid set of chromosomes
3) The tip of the nucleus is covered by the acrosome, a protein-filled vesicle containing enzymes to penetrate the egg
4) Most of the tail is flagellum - a group of contractile filaments that produce whiplike movement capable of propelling the sperm at velocity
5) Mitochondria form the midpiece of the
sperm and provide the energy for movement

205
Q

HPG axis of male reproductive system

A

1) Gonadotropin releasing hormone (GnRH) secreting neuroendocrine cells of the HYPOTHALAMUS
2) The GnRH travels to the anterior pituitary via the hypothalamo-hypophyseal portal vessels and triggers the release of both LH & FSH
3) FSH primarily acts on the Sertoli cells to stimulate the secretion of paracrine agents required to initiate SPERMATOGENESIS

4) LH acts primarily on the Leydig cells to stimulate TESTOSTERONE secretion:
- Testosterone (in addition to its many systemic
effects as a hormone) acts locally by diffusing
from the interstitial spaces into the
seminiferous tubules
- Testosterone then enters Sertoli cells where it
is able to facilitate SPERMATOGENESIS

206
Q

Negative feedback in the HPG axis in male RT

A

Testosterone INHIBITS LH secretion in two ways:

  1. Acts on the hypothalamus to decrease the amplitude of GnRH bust resulting in a decrease in the secretion of GnRH
  2. Acts directly on the anterior pituitary gland to decrease LH only

Sertoli cells (stimulated by FSH) release a protein hormone called INHIBIN which acts on the anterior pituitary to inhibit the release of FSH only

207
Q

Before puberty

  • What are the levels of GnRH and GHRH?
  • Consequences of this
A
  • Low levels of GnRH & GHRH (growth hormone releasing hormone) secretion from the hypothalamus
  • Low levels of anterior pituitary; FSH, LH, GH (growth hormone) & gonadal sex steroids
208
Q

At puberty

  • What are the levels of GnRH and GHRH?
  • Consequences of this
A
  • Increase in the levels of GnRH & GHRH

- Increase in FSH, LH, GH & sex steroids

209
Q

Normal puberty is driven by what and what is it also influenced by?

A 
Centrally driven and dependent on an intact hypothalamic-pituitary gonadal axis
- Influenced by many other factors:
• Nutrition
• Insulin
• Genetic factors
• Exercise
210
Q

What are the main physical changes in a male in puberty? When do these changes appear?

A
  • Starts at 9-14 years (average is 12)
  • 1st sign - testicular enlargement
  • Pubic, axillary (armpit) & facial hair growth
  • Growth spurt
  • Spermatogenesis begins
  • Acne, body odour & mood changes
211
Q

What are the main physical changes in a female in puberty? When do these changes appear?

A
  • Starts at 8-14 years (average is 11)
  • 1st sign - breast development
  • Pubic & axillary hair growth
  • Growth spurt (not as large as males though)
  • Menarche (first menstruation - 2.5 years after start of puberty)
  • Acne, body odour & mood changes
212
Q

Menopause

A

The cessation of menstruation, usually occurring between 48-52 years, when the ovaries STOP releasing eggs.

213
Q

Mechanism of menopause

A
  1. Depletion of primordial follicles - occurs at around 40 yrs
  2. Decrease in follicular oestrogen production
  3. Gradual increase in FSH & LH (due to the lack of negative feedback provided by oestrogen)
  4. Decline of inhibin resulting in a further increase in FSH
  5. Increase in FSH results in the rapid increase in oestrogen secretion from existing follicles
  6. Results in shorter menstrual cycles
  7. As fewer follicles remain, the increase in FSH no longer stimulates the increase in oestrogen - occurs at 6-12 months pre-menopause
  8. The decrease in oestrogen and lack of ova results in menopause
214
Q

Short term signs of menopause

A
  • Hot flushes, sweats, palpitation, headaches
  • Irritability, lethargy (lack of energy), panic attack & depression
  • Shorter menstrual cycle
  • Altered blood loss
  • Skin dryness
215
Q

Long term signs of menopause

A
  • Vaginal dryness - resulting in painful intercourse
  • Decrease in libido
  • Hair loss/thinning
  • Diminished urethral seal and loss in compliance
  • General aches and pains
216
Q

Osteoporosis and menopause

A

Women are more at risk of developing osteoporosis than men because of the hormone changes that occur in menopause directly affect bone density –

Oestrogen is essential for healthy bones, after menopause, oestrogen levels drop resulting in a rapid decrease in bone density.

217
Q

What is defined as premature menopause?

What are some causes of this?

A
  • Before the age of 40
  • Idiopathic.
  • Iatrogenic (result of diagnostic and therapeutic procedures)
  • Chromosomal (fragile X syndrome, FMR1)
  • Autoimmune.
218
Q

Other long term risks in menopause

A

Cardiovascular disease

Breast cancer

219
Q

At birth how many eggs do the ovaries contain?

A

2-4 million eggs (no new ones appear after birth)

220
Q

Describe what happens in early fetal development that forms the primary oocytes.

A
  • During early fetal development, the primitive germ cells, or oogonia undergo numerous MITOTIC DIVISIONS:
  • Oogonia are homologus to the spermatogonia in males
  • Around the 7th month of gestation, the fetal oogonia STOP dividing
  • During fetal life all of the oogonia DIFFERENTIATE into PRIMARY OOCYTES (analogous to primary spermatocytes)
221
Q

When does meiosis 1 take places in primary oocytes?

What is meiotic arrest?

A
  • Meiosis 1 begins in-utero before 12 weeks
  • Recombination & crossing over occurs
  • However meiosis is ARRESTED at metaphase 1 until PUBERTY - known as MEIOTIC ARREST
222
Q

When is meiosis 1 completed in the primary oocyte to form secondary oocyte?

A
  • Resumption of meiosis 1 occurs after puberty
  • Meiosis 1 is completed just before ovulation:
  • This division is analogous to the division of the primary spermatocyte in that each daughter cell receives 23 chromosomes, each with two
    chromatids
  • However, in this division, one of the two daughter cells - the SECONDARY OOCYTE, retains virtually ALL of the cytoplasm
  • The other daughter cell is the first polar body and is very small non-functional
223
Q

Describe the events of meiosis 2 in the secondary oocyte. When does it happen?

A

MEIOSIS 2 occurs whereby the secondary oocyte develops into the OVUM

  • The daughter cells each receive 23 chromosomes each with a single chromatid
  • Meiosis 2 is also ARRESTED at metaphase 2 until FERTILISATION
  • Meiosis 2 is only completed in the fallopian tube AFTER FERTILISATION (penetrated by sperm)
  • One daughter cell now called the OVUM retains nearly all of the cytoplasm
  • The other daughter cell, the second polar body is very small and nonfunctional
224
Q

How many ovum’s does each primary oocyte produce?

A

The net result of oogenesis is that each primary oocyte can produce only ONE OVUM

225
Q

What are the three main differences between oogenesis and spermatogenesis?

A

1) 1 spermatocyte -> 4 spermatozoa whereas 1 oocyte -> 1 ovum
2) Both maturations occur in testis whereas one occurs in ovaries and one in the
fallopian tube after fertilisation
3) Continuous process whereas disjointed process (days-years)

Phase 1 revision (5 decks)

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