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203 - Theme 1 - The Endocrine System > L12 - Endocrinology of ageing > Flashcards

L12 - Endocrinology of ageing Flashcards

1
Q

Evolutionary perspective

A

We are outliving our natural lifespan

Hormonal function:

  • menopause
  • andropause
  • somatopause
  • adrenopause
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2
Q

Cultural perspective

A

Anti-aging results in 2,940,000 google hits

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3
Q

Pharma perspective

A

Enormous market

-especially compared to ‘endocrine’ market for testosterone/GH

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4
Q

What is meant by ‘medicalisation’ of ageing?

A

Increased life expectancy may not equate to increased health expectancy

It is important to balance the benefit and harm of treatment
-especially cancer risk in elderly

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5
Q

Association and causation

A 
Similar phenotypes:
-hypogonadism/growth hormone deficiency/ageing
=>^ fat mass ^ visceral fat
=>sarcopenia
=>decreased bone mineral density
=>decreased mood/QOL
=>^ risk CVD

Phenotypes are :

  • non-specific
  • high prevalence
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6
Q

Age: Nutritional status

A

Weight

  • increases from mid 30s
  • to 50-70yrs

Lean body mass
-decreases 6-8%/ decade from mid - 30s

Diet
-trend towards decreasing intake total energy and protein with increasing age

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7
Q

Age: insulin/glucose

A

increased insulin and glucose with increasing age

increases insulin resistance

decrease in peripheral glucose uptake

increase in prevalence of metabolic syndrome with increasing age

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8
Q

What is metabolic syndrome?

A

Constellation of closely associated CV risk factors

  • visceral obesity
  • dyslipidaemia
  • hyperglycaemia
  • hypertension

Insulin resistance is the underlying pathophysiological mechanism

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9
Q

Age: menopause definition

A

Menopause=ovarian failure

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10
Q

Oestrogen levels pre and post menopause

A

pre-menopausal: cycling

post-menopausal: very low constant levels
-decreased oestrogen, increased FSH and LH

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11
Q

Symptoms of menopause

A

hot flushes

night sweats

median duration of menopausal symptoms is 7 years

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12
Q

Age at menopause

A

approx 50 +/- 2 yrs

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13
Q

Morbidity associated with menopause

A

increased risk of osteoporosis, CHD and sexual dysfunction

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14
Q

Post-menopausal HRT: risks v benefits?

A

Initial observational studies showed benefits
-healthy user bias

Some subsequent RCTs showed no benefits and increased risks

However risk:benefit ratio depends on

  • other risk factors
  • age of woman and duration of HRT use
  • greater risk if >60yrs, >10yrs post-MP
  • type of HRT (oestrogen, progesterone, route)
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15
Q

Benefits of post-menopausal HRT

A

Rx menopausal Sx

Decreased osteoporosis/fracture risk
-for duration Rx

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16
Q

Risks of post-menopausal HRT

A

Increase venous thromboembolism

Increase breast cancer (small)
-esp > 5 years

Increase endometrial cancer
-if use unopposed oestrogen

17
Q

Goal of post-menopausal HRT

A

shifted back from ‘replacement’ (to prevent disorders associated with post-menopausal oestrogen deficiency, like osteoporosis) to ‘treatment’ of menopausal symptoms
-short term, lowest effective dose, younger menopausal women

18
Q

Male gonadal axis

A

Gradual decrease in testosterone with increasing age

Wide range of normality at all ages

At 75yrs, mean testosterone approx 2/3 of that at 25yrs

Poor association between libido/erectile dysfunction and testosterone

Testosterone prescriptions increased by 500% over the past decade

19
Q

Clinical hypogonadism

A

decreased sexual function

increase osteoporosis

decreased muscle strength

20
Q

Testosterone treatment: Bones

A

increase bone mineral density if hypogonadal

? effect on fracture risk ?

bisphosphonates work, independent androgen status

21
Q

Testosterone treatment: body composition

A

increase lean body mass

decreased fat mass

no convincing functional benefits demonstrated

increase muscle strength with supra-physiological doses

22
Q

Testosterone treatment: benefits and risks

A

Little/no evidence of benefit/insufficient data

  • atherosclerosis/coronary artery disease
  • sexual function
  • most erectile dysfunction is atherosclerotic
  • drugs like sildenafil (viagra) may work
  • cognitive function
  • mood/ QOL

Risks

  • prostate (benign prostatic hypertrophy/cancer)
  • erythropoeisis (increased haematocrit)
  • ? cardiovascular risk ?
23
Q

Effect of weight loss on testosterone

A

increase in total testosterone when increase in body weight loss

positive correlation

24
Q

GH treatment

A

Body composition

  • increased lean body mass approx 2kg
  • decreased fat mass approx 2kg
  • no convincing functional benefits demonstrated

No significant change

  • bone mineral density
  • lipids
25
Q

Potential risks and side-effects of GH treatment

A

Potential risks
-increases risk of cancer: increases [IGF-1] in observational studies is associated with increase risk of non-smoking cancers such as prostate, colon and breast

Side-effects

  • soft tissue oedema
  • arthralgias
  • carpal tunnel syndrome
26
Q

Age: cortisol

A

↑ trough levels cortisol with ↑ age

↑ average levels cortisol with ↑ age

Phase advance of diurnal rhythm
-Time at trough and peak both earlier

27
Q

DHEA

A

decline in men and women with age

28
Q

Regulation/action of DHEA

A

? ACTH +
? Action via androgen and/or oestrogen R ?
-‘Pro-hormone’
-Potential for adverse effects of treatment (prostate, breast) –
not demonstrated

29
Q

Importance of DHEA in men

A

Overwhelming excess of more potent circulating androgens

Contribution to androgenic effects in men ‘modest’ at most

30
Q

DHEA in USA

A

Regulated by FDA

A food supplement, not a drug

Readily available

Decreased regulation

  • Claims may be unsubstantiated
  • Composition varies
  • May contain 0 - 15% of amount stated on packet
31
Q

DHEA benefits and adverse effects?

A

No evidence of beneficial effects on

  • Body composition
  • Physical performance
  • Insulin sensitivity
  • QOL

No adverse effects demonstrated

Multiple studies have not demonstrated any positive effect of DHEA in ageing individuals

No evidence for use

32
Q

Age: thyroid function

A

Slight increase [TSH] with age
T4 →
↓ peripheral T4 → T3 conversion with age
↓ [T3] with age

No evidence for beneficial effect of T4 treatment!
May do harm
?↑ risk osteoporosis, atrial fibrillation
? risk in elderly with atherosclerotic coronaries

33
Q

Starvation/AN: insulin, glucose and leptin

A

↓ insulin, ↓ glucose, ↑ insulin sensitivity

LEPTIN
-Produced by white adipose tissue
[leptin] correlates with BMI and body fat
-Reports nutritional information to the hypothalamus
-‘Starvation signal’: signals energy availability
↓[leptin] ↑ food intake, ↓ energy expenditure,
↓[leptin] ↓ fertility
-Permissive factor for initiation of puberty

34
Q

STARVATION / AN:

oestrogen / testosterone

A 
↓ LH, ↓ FSH, 
↓ oestrogen / testosterone
↓ fertility, amenorrhoea
‘hypothalamic amenorrhoea’
makes ‘evolutionary sense’ in times of famine
Osteoporosis
Rx HRT / COCP
35
Q

Links between metabolism and reproduction

A

Ob Ob mouse:
-Hyperphagic & obese

ALSO
Low gonadotrophins
Incomplete development of reproductive organs
Does not reach sexual maturity
Infertile

Leptin Rx:
-Reduce obesity

ALSO
Restore Gn secretion
Mature gonad
Induce puberty
Restore fertility
36
Q

Central mediator: kisspeptin

A

A GnRH secretagogue

KISS1 neurons highly responsive to oestrogen, implicated in both + and – central feedback of sex steroids on GnRH production

Metabolic influences on reproduction mediated by leptin via the kisspeptin system

  • Puberty
  • Reproduction
37
Q

STARVATION / AN: GH / IGF axis

A

‘GH resistance’
↑ GH, ↓ IGF-I

Seen in acute starvation and in AN

? down-regulation hepatic GH receptor and / or post-receptor defect

Reversible with re-feeding

38
Q

STARVATION / AN: CORTISOL

A

look at graphs

39
Q

STARVATION / AN:

THYROID FUNCTION

A

TSH and T4 lower limit of normal

↓ T4 conversion to T3 ↓ T3 (active)

↑ T4 conversion to rT3 ↑ rT3 (inactive)

Consequences

  • Lower basal metabolic rate
  • Conserve energy

203 - Theme 1 - The Endocrine System (11 decks)

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