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Sem 1 Year 2 > Transitions > Flashcards

Transitions Flashcards

1
Q

What is meant by transitions?

A

‘Changes that arise in health (or illness) or development, as well as the efforts of the individuals undergoing the transition to adapt and regain normality’

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2
Q

What is meant by trajectories?

A

Long term patterns of stability and change, often including multiple transitions

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3
Q

What are the 3 main trajectories of life?

A
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4
Q

What is ossification and what are the two types?

A

Ossification= any process that results in formation of solid bone
Endochondral ossification and intramembranous ossification

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5
Q

What happens after bone is initially created?

A

It goes through remodelling, where woven bone becomes lamellar bone

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6
Q

What is the difference in endochondral and intramembranous ossification?

A

Endochondral= bones grows onto pre-existing scaffold, process that occurs in the physics of long bones
Intramembranous= occurs when osteoblasts lay down osteoid within a fibrous membrane, occurs in flat bones

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7
Q

What happens during growth from the physics plates?

A
  • Chondrocytes transition through a cascade of stages; growing in number, then size, then undergoing apoptosis to release their stored calcium
  • In the primary spongiosa, osteoprogenitor cells invade this calcified matrix, laying down woven bone which is then remodelled in the secondary spongiosa to lamellar bone.
  • There is a physis at each end of the long bone- growth in two directions usually happens at different rates
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8
Q

When is peak height velocity in girls and boys?

A

Girls- just before 12, boys- just before 14

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9
Q

What are the 3 main stages of growth?

A

Foetal, affected by uterine environment and nutrition provided
Infantile, dependant on nutrition and disease
Childhood growth, slow and long- genetics have an impact
Puberty- lasts until the end of growth

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10
Q

What is childhood growth like?

A

Childhood growth is slow but long, genetics have an impact. Growth hormone is needed (affects the physis) and thyroid hormones, Vit D and steroids. Profound psychological unhappiness can decrease growth hormone secretion

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11
Q

What is pubertal growth like?

A

Puberty- lasts until end of growth in the mid-late teens; sex hormones (testosterone and oestradiol) cause the back to grow, boost GH to be released and eventually cause fusion of the epiphyseal growth plates

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12
Q

When is the fastest period of growth?

A

Foetal

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13
Q

How does the onset of puberty occur?

A
  • The hypothalamus starts a pulsed secretion of Gonadotrophin‐ releasing hormone, also known as GnRH.
  • Happens each night- initially weak and not for long but eventually longer until the hormone is being released all the time
  • GnRH stimulates the pituitary gland to release FSH and LH which then then travel to gonads to trigger release of androgens
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14
Q

When does puberty start for girls and boys?

A

8-13 for girls
9-14 for boys

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15
Q

What are the effects of testosterone on pubertal boys?

A

Muscle mass increases- bulk and strength
Bone density to increase and grow in certain areas e.g. shoulders
Causes sex organs to start maturation
Increases hair growth

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16
Q

What is the main driver of physical closure in boys?

A

Testosterone

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17
Q

What happens to fat distribution in females who undergo puberty?

A

There is changes- covering hips, buttocks and thighs and also leading to more subcutaneous fat in face
Females end up with a body fat percentage twice that of males

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18
Q

What are the effects of oestrogen in pubertal girls?

A

Triggers fat distribution change
Causes bone density to increase as well as a widened pelvis
Causes sexual maturation of organs
Great growth and feeding function

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19
Q

What is adrenarche?

A

The pubertal awakening of the adrenal gland

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20
Q

When does adrenarche occur?

A

~ 2 years before gonadarche

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21
Q

What happens during adrenarche?

A

Zona reticularis develops and adrenal androgens start to be produced from adrenal androgen precursors (DHEA, DHEA-S and androstenedione)
Causes physical signs include axillary odor, acne and pubic/axillary hair

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22
Q

When does clinically evident development of pubic hair appear?

A

Around gonadarche (puberty)

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23
Q

What occurs during gonadarche?

A

There is increased pulsatile release of GnRH, from hypothalamus which causes increased pituitary release of gonadotrophin LH and FSH
This is when breast development/ teste development and growth of ovaries due to estradiol progesterone and testosterone
Secondary sex characteristics

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24
Q

What is pubarche?

A

Development of pubic hair between adrenache and gonadarche

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25
Q

What is thelarche, menarche and spermarche?

A
  • Thelarche, onset on female breast development, usually first sign of puberty in girls
  • Menarche, onset of menstruation, around 2 years after thelarche
  • Spermarche is the onset of sperm emission
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26
Q

What do the graphs of GnRH, responsiveness of the HPG axis and plasma LH and FSH look like during puberty?

A
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27
Q

When are the 3 peaks of HPG activity during an individuals lifetime?

A
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28
Q

What is the purpose of mini-puberty?

A
  • Mini puberty- transient postnatal HPG axis activation and sex steroid surge, not well understood
  • Influences reproductive organ development, body composition and growth, cognitive functions and behaviour
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29
Q

What causes the initiation of puberty?

A

Puberty is initiated with a sustained in pulsatile GnRH release
Neurotransmitters can modify the GnRH secretory pattern, with excitatory or inhibitory effects
During childhood an inhibitory network is the predominant pathway, the inhibitory network decreases around the time of puberty initiation

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30
Q

What protein release plays a key role in controlling pubertal onset?

A

Kisspeptin

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31
Q

What is a KNDy neurone and what does it stimulate?

A

Kisspeptin, neurokinin B and dynorphin form a neuronal ensemble (KNDy neuron)
They send stimulatory signals to GnRH neurones to generate a pulsatile secretion pattern.
Binds to G-protein coupled receptors to initiate a series of downstream events

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32
Q

What is the difference in response to kisspeptin in males and females?

A

There is different responses to kisspeptin in male and females; kisspeptin stimulates the release of LH in males, its effect is more variable in females dependent on the phase of the menstrual cycle

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33
Q

What are the hypothesis for what controls kisspeptin biosynthesis and secretion?

A
  • Hypothesis 1= pubertal clock
  • Hypothesis 2= the attainment of particular state of somatic maturation e.g. reaching a certain body fat level
34
Q

What reduces and increases gonadotrophin inhibiting hormone?

A

Increased melatonin increases inhibiting hormones and increased leptin reduces GnIH

35
Q

What can inhibit the release of KNDy neurone?

A

Inflammation, sex steroids, stress, drugs e.g. opioids and metabolism

36
Q

What is precocious puberty and what can cause it?

A

Early development of secondary sexual characteristics before 8 in girls and 9 in boys
Can be a variant of normal development, or due to McCune-Albright syndrome, gonadotrophin secreting tumours or exogenous sex hormone

37
Q

What is delayed puberty and what are the causes?

A

Absence or incomplete development of secondary sexual characteristics by 13 years in girls, 14 years in boys
Causes can be variant of normal development, hypogonadotrophic hypogonadism, hypopituitism, chromosomal abnormalities or hypothalamic dysfunction due to secondary causes

38
Q

What is contrasexual development and what are common causes?

A

When male or female children develop physical features of the opposite gender
Common causes are polycystic ovaries and increased adrenal gland responses

39
Q

What are terms used where a person is born with an anatomy that does not align with our assumptions about male and female?

A
  • Intersex
  • Person with diverse sex characteristics (DSC)
  • Person with differences of sex development (DSD)
40
Q

What is the difference in gender identity and expression/presentation?

A
  • Gender identity= a person’s internal sense of their own gender; the gender we feel and experience ourselves to be
  • Gender expression or presentation= how we express and present our gender to others and to ourselves, through e.g. clothing, mannerisms, and social gender roles
41
Q

What is trans broken arm syndrome?

A

Trans broken arm syndrome- healthcare providers assume that any health issue a trans patient may present with is a result of their trans status and/or gender affirming hormone treatment.

42
Q

What is the menopause?

A

Permanent cessation of menstuation, there is loss of ovarian follicular activity as a women ages, leading to a decrease in both quality and quantity of oocytes- this then leads to the loss of ovarian hormonal function

43
Q

How can women who has undergone the menopause still become pregnant?

A

Need donor eggs and exogenous hormone stimulation

44
Q

What are the symptoms and long term effects of the menopause?

A
45
Q

What is normal menopausal and abnormal ages?

A

Average age= 51, typical range is 45-55 years
Abnormal is < 40 years. Can be due to primary ovarian insufficiency or premature ovarian failure

46
Q

What are some of the factors that affect menopausal age?

A
  • Genetics and ethnicity
  • Smoking/ substance abuse
  • Reproductive history
  • Chemotherapy or pelvic radiation
  • Oophorectomy or hysterectomy
47
Q

What is the pattern of estrogen level throughout a women’s life?

A
48
Q

What is normal oocyte count for women throughout their life?

A
49
Q

What do postmenopausal ovaries produce and what is it converted to?

A
  • Postmenopausal ovaries produce androstenedione and testosterone
  • These androgens are converted in fat, muscle and skin into estrone, a weak estrogen
50
Q

What is high levels of estrogen linked with?

A

Endometrial and breast cancer

51
Q

Why do menstrual cycles become shorter just before the menopause?

A
  • This is due to the smaller, less functional follicles producing lower levels of estradiol inhibin and anti-mullerian hormones which leads to increased FSH secretion and a subsequent overshoot of estradiol production, facilitating and accelerating the LH surge
  • This in turn results in accelerated ovulation and shortened follicular phases
52
Q

Why do FSH levels rise in post-menopause and perimenipasual women?

A

When the ovaries are depleted of follicles and estradiol, inhibin and AMH levels fall, there is loss of negative feedback on the HPG axis, resulting in increased production of GnRH
This leads to menstruation no longer taking place

53
Q

The decline in what hormones explains why fertility is impaired in women before cycle disruption?

A

Inhibin B and AMH

54
Q

What are the changes in hormones (FSH, LH, estradiol and inhibit B) seen in reproductive and menopausal women?

A

15 fold increase in FSH and 10 fold in LH

55
Q

What are vasomotor symptoms and how long do they last?

A

Vasomotor symptoms (80% experience these)= hot flushes, night sweats, cold sweats, heart palpitations and changes in blood pressure
These symptoms are severe but tend to stop after a couple of years.

56
Q

What is thought to cause vasomotor symptoms?

A

Thought to be due to abrupt drop in estrogen levels affecting the hypothalamic thermoregulatory centre

57
Q

What is the function of the lower genital tract dependant on?

A

Estrogen

58
Q

What are the effects of the menopause on the lower genital tract and how long do they last?

A

Tissues lining the vagina, vulva, bladder and urethra undergo atrophy. Can cause vaginal dryness, painful intercourse, dry skin around the vulva and recurrent urogenital infections
These symptoms can persist throughout menopausal life

59
Q

How does lower estradol affect the body in general?

A

Affects cardiovascular and bone health
Lowers metabolic rate- tend to have increased visceral fat
Also causes less muscle mass

60
Q

How do you diagnose menopause in women over 45, and women under 45?

A

Over 45 with menopausal symptoms= diagnose on tests alone
Under 45 with menopausal symptoms= check FSH levels

61
Q

What FSH levels indicate menopause?

A
  • Serum FSH > 30 iU/L is consistent with perimenopause, but does not confirm that the individual has has their final period
  • Normal FSH does not exclude perimenopause has it fluctuates so much
62
Q

What are some of the risks of HRT?

A

Risk of breast cancer, ovarian cancer and thrombosis

63
Q

How can the risk of thrombosis in HRT be reduced?

A

Stop oral HRT and give transdermal HRT

64
Q

What hormones are included in HRT and why?

A

Estrogen to help with symptoms
But this on its own can cause cancer- progesterone is also given to protect the endometrium from estrogen

65
Q

How are hormones given to a perimenopausal women who has had recent menstruation?

A

Estrogen all the time
Progesterone 14 days on, 14 off. Causes a bleed. If tried to give progesterone solidly whilst still have some ovarian function, can end up with chaotic bleeding
Called sequential HRT

66
Q

What are the risks of transdermal testosterone?

A

Low dose transdermal testosterone is increasingly used, but is often ineffective, has side effects (acne/ hirsutism/ alopecia/ irritability) and unknown about long term safety

67
Q

How do you manage urogential atrophy?

A

Low dose estrogen as a cream or vaginal tablet so little of it is absorbed systemically

68
Q

Is HRT a contraceptive?

A

No

69
Q

What are some non-pharmacological menopause management options?

A
  • Avoid vasomotor triggers (caffeine, hot drinks, alcohol)
  • Layer clothing and bedding
  • Mindfulness/ CBT
  • Exercise- weight bearing important for OP
  • Sleep apps
  • Lubricant and vaginal moisturiser
70
Q

What are other non-HRT medication that can be given to help alleviate menopause symptoms?

A

SSRI/SNRI/gabapentin/oxybutynin

71
Q

What side effect of menopause is oxybutynin used to help?

A

Used for sweats but can cause dry mouth/eyes

72
Q

What are the main positives with HRT?

A

Can reduce the risk of cardiovascular and osteoporotic risks
Can lessen the symptoms in some women

73
Q

What percentage of women use complementary and alternative medicines for menopause symptoms?

A

50%

74
Q

What are the 4 main types of bone cell?

A
75
Q

What causes osteoclast progenitors to fuse together and migrate to the site of bone resorption?

A

RANKL- binds to to RANK receptor on their surface

76
Q

What released RANKL and what regulates it?

A

Released by osteocytes and osteoblasts and is regulated by the local mechanical environment and systemic release of parathyroid hormone

77
Q

What molecule inhibits bone resorption?

A

Osteoblasts also release OPG which irreversibly binds to free RANKL, preventing it from binding to osteoclast precursor

78
Q

How does calcitonin and parathyroid hormone affect bone remodelling?

A
  • Calcitonin from the thyroid has a direct inhibitory effect on OC- inhibits bone resorption.
  • PTH triggers an increase in RANK‐Ligand secretion by osteoblasts leading to more bone breakdown by osteoclasts and therefore an increase in serum calcium.
79
Q

What occurs in bone remodelling?

A

Osteoclasts remove the bone then undergo apoptosis, then osteoblasts lay down new osteoid which is later mineralised to solid bone

80
Q

What is the graph of bone mass against age?

A
81
Q

What causes peak bone mass to decrease after 40?

A

After 40, bone mass decreases due to a reduction of estrogen levels and testosterone levels (testosterone is broken down to estrogen in males)

82
Q

How does estrogen affect bone mass?

A

It has a protective effect
- Estrogen acts directly on the OBs to limit the amount of RANKL released, so limiting the signalling for osteoclasts to be made
- Means rate of construction and demolition is roughly equal
- Inhibitory action is lost after estrogen declines during and after menopause. Lose the equilibrium

Sem 1 Year 2 (18 decks)

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