Weeks 9,10&11 Transitions Flashcards

1
Q

Effects of testosterone at puberty

A
  • ‘Male traits’
  • Bone density/growth
  • Density greatly increases
  • Disproportionate (facial, shoulder
    width)
  • Muscle mass
  • Increases bulk and strength
  • Main driver of physeal closure in
    males
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2
Q

Endochondral vs Intramembranous ossification

A

Endochondral ossification
* Occurs on a cartilage scaffold
* Most of the skeleton
* The physis
* Fracture healing (cast)

Intramembranous ossification
* Embryonic flat bones
* Subperiosteal bone growth
* Fracture healing (plate/screws)

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3
Q

Main effects of oestrogen in females

A

‘Female traits’
* Fat distribution
* Buttocks, hips, thighs
* Facial subcutaneos fat
* Bone density/growth
* Increase density
* Widened pelvis, anteverted hips

  • Main driver of physeal closure in
    females
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4
Q

What are the two stages of puberty?

A

Adrenarche - Awakening of the adrenal gland

  • Adrenal androgen precursor secretion (DHEA, DHEA-S, and androstenedione)
  • Physical signs include pubic/axillary hair development, axillary odor, and acne

Gonadarche (8-14 years): onset of true central puberty

Increased pulsatile release of GnRH from the hypothalamus
Increased pituitary release of gonadotropins LH and FSH

Breast development and growth of ovaries (estradiol and progesterone production);
Growth of testes (testosterone production)

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5
Q

What physical signs are associated with adrenache and gonadarche?

A

Adrenarche: pubic/axillary hair development, axillary odor, and acne

Gonadarche: effects of oestrogen and testosterone

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6
Q

What is meant by mini-puberty?

A

This is the second awakening of the HPG axis and occurs in infancy

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7
Q

What initiates pubertal onset?

A

Puberty is initiated with a sustained increase in pulsatile GnRH release from the hypothalamus

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8
Q

Which hypothalamic structure plays a key role in pubertal control?

A

Hypothalamic kisspeptin release plays key role in controlling pubertal onset

Kisspeptin binds to the G-protein coupled receptor (KISS1R) expressed by GnRH neurons, to initiate a sequence of downstream events

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9
Q

What is the main factor of pubertal onset?

A

Genetics

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10
Q

What metabolic factor has an influence on pubertal onset?

A

Leptin

Appears to play a permissive role in puberty initiation and maintenance
of reproductive function

Earlier initiation of puberty seen in obese children may be partly explained by higher leptin levels

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11
Q

What neuron produces kisspeptin?

A

KNDy neuron

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12
Q

What is precocious puberty and what is the age definition?

A

Precocious puberty: early development of secondary sexual characteristics before 8 years
in girls, 9 years in boys

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13
Q

What might enduce precocious puberty?

A

Benign premature adrenarche, CNS or pituitary lesions, McCune-Albright syndrome,
gonadotropin-secreting tumours or exogenous sex hormones, congenital adrenal hyperplasia (increased androgens)

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14
Q

What is the definition of delayed puberty?

A

Delayed puberty: absence or incomplete development of secondary sexual characteristics
by 13 years in girls, 14 years in boys

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15
Q

During puberty what might cause contrasexual development?

A

Contrasexual development

  • More prevalent in girls due to endogenous androgen production existing anyway. Examples are polycystic ovaries, increased adrenal gland responses such as congenital adrenal hyperplasia

Less common in boys, typically caused by estrogen-secreting tumours

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16
Q

How do puberty blockers work?

A

They are GnRH agonists.

Naturally GnRH is pulsile so by applying a constant does the pituitary becomes desensitised and stops reacting to it and stops releasing LH and FSH

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17
Q

What are the three signals used in bone resorption?

A

RANKL - released by osteoblasts and osteocytes, promotes osteoclast resorption.

OPG - released by osteoblasts, binds to RANKL thus inhibiting resportion

PTH - parathyroid hormone - stimulates osteoblasts to release RANKL

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18
Q
A
19
Q

Draw out the calcium homeostasis loop

A
20
Q

What is the rough timeline of bone mass?

A

Peak: 27
Platau: 27-40
Decline: 40 onwards
Menopause: 46 increased decline

21
Q

Two very common insufficiency fractures seen in women over 60

A

On the left is a distal radius fracture and in this case a Colle’s fracture

And on the right a proximal humerus fracture.

Both of these are usually sustained in a simple fall, like tripping over a rug

22
Q

What is oestrogen’s role in preventing osteoporosis?

A

Oestrogen inhibits oscteoclasts.

It limits the amount of RANKL that osteoblasts release and promotes OPG synthesis.

Without this osteoclast scranning outdoes osteoblast cooking and there’s no food left

23
Q

What is the definition of osteoporotic bone?

A

A decrease in bone density.

Osteoporotic bones have normal bone quality, present in reduced quantity.

Osteoclasts scran bone like saz scrans cheese, not from the edge, indiscriminantly.

24
Q

Symptoms of menopause

A
25
Q

Average age of menopause

A

Average age 51 years

Typical range 45–55 years

26
Q

What age is considered abnormal menopause

A

< 40 years

27
Q

What is the difference between primary ovarian insufficiency and premature ovarian failure

A

Primary ovarian insufficiency:
* Altered, suboptimal ovarian function and hormone production

Premature ovarian failure:
* Ovaries fully stop functioning

28
Q

Hormone’s that decrease in menopause that normally negatively feedback on the hypothalamus and pituitary?

A

Oestrogen, Inhibin, aMH

29
Q

What is the telltale hormonal sign of menopause?

A

Increased FSH.

This is noticed before any mentrual symptoms.

I assume we use this over oestrogen because it is affected by all three inhibiting hormones so has the most significant change.

30
Q

Anatomical changes that occur in the female reproductive system during menopause.

Think

  • Ovaries
  • Opening of Cervix
  • Vagina
  • Uterus
  • Fallopian tubes
A
31
Q

What is the cause of the temperature regulation symptoms of menopause?

A

Vasomotor symptoms:

Abrupt drops in estrogen levels disrupt hypothalamic thermoregulatory centre

Results in miscommunication between brain and vascular system

Rusults in disruption of core body temperature and
normal temperature responses

32
Q

Cardiovascular effect of menopause?

A

Cardiovascular disease

Explaination:

Estrogens promote vascular remodelling + elasticity,
regulate reactive dilation and local inflammatory activity

Loss of estrogen may lead to impaired endothelial function and vascular changes

33
Q

What is the menopausal effect on metabilism

A

Decreases

Metabolic consequences:

Loss of estrogen associated with metabolic changes
and lower metabolic rate

Menopausal women have increased visceral fat and
adverse lipid profiles

34
Q

What are the contraindications of menopausal hormone replacement therepy?

When would you give it?

When might you give it?

When would you definitely not?

A
  • Risk of breat cancer or endometrial cancer
  • Risk of CVD
  • Active liver disease
  • Undiagnosed vaginal bleeding
35
Q

What are the serum FSH levels consistent with perimenopause?

A
36
Q

What hormones does menopausal HRT consist of?

A

estrogen for symptoms
progestogen to protect endometrium from estrogen

37
Q

What is the HRT regime for menopause in:

Women without a uterus (and no endometriosis)

Women with a uterus but recent mentrusation

With with a uterus and longer since mentstruation

A

Mirena is the coil

38
Q

What is the treatment for menopausal loss of libido?

A

None

Testosterone can work but has too many side effects

39
Q

Treatments for urogenital atrophy

A

Vaginal lubricant
Estring (sits in vagina and give a slow release of estrogen)

40
Q

In H&E which stains the the nucleus and which stains the cytoplasm?

Which stains acidic substances and which is an acidic stain?

Which is pink and which is purple?

A

Haematoxylin is a basic stain which stains the acidic components in the cell, such as the nuclear DNA. Purple

Eosin being an acidic stain, stains the basic components of
the cytosol. Pink

41
Q

What is the mechanism by which oestrogen inhibits osteoclast activity?

A

It inhibits the release of RANKL by osteoblasts

42
Q

What is McCune-Albright syndrome (MAS)

A

Genetic dissorder which causes early puberty, brittle bones, cafe-au-late marks and hyperthyroidism

43
Q

What is oestrogens relationship to CVD?

A

Complicated, it provides protection against the CVD effects of testosterone hence increased risk of CVD post menopause

However it is also the cause of CVD side effects in the combined pill.