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Endocrinology > Obesity, PCOS, amenorrhoea > Flashcards

Obesity, PCOS, amenorrhoea Flashcards

1
Q

Why do we want rapid weight loss before bariatric surgery?

A

Ideally 8 weeks of VLCD

Shrinks the liver and makes the procedure safer

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2
Q

List potential weight loss drugs

A

Phentermine

Locaserin

Natrexone/bupropion

Topiramate

Liraglutide (GLP1 agonist)

In T2DM, metformin, SGLT2i and GLP1 agonist have weight benefits

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3
Q

What’s the gold standard for bariatric surgery?

A

Gastric bypass

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4
Q

Benefits and downfalls of gastric bypass

A

Gold standard

Benefits
Completely reversible
Good at reversing diabetes if done within 8 years of diagnosis
40% reduction in all cause mortality (CAD, diabetes, cancer)

Downfalls
Need to take lifelong iron and vitamins
Lifelong monitoring
Rapid absorption with ETOH 
Rapid bone loss in the first 2 years --> OP (ensure calcium and vitamin D are adequate)
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5
Q

Downfalls of gastric banding

A

Lots of reflux
Permanent damage to the proximal portion of stomach and oesophagus

Not very good at reversing OSA or T2DM

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6
Q

Benefits and downfalls of gastric sleeve

A

Benefits
Easier to do in obese people, laparoscopic procedure

Downfalls
Permanent
Tubular stomach that remains can dilate and lead to weight gain again
Reflux
Nutritional insufficiency (but not as bad as gastric bypass)
Rapid absorption of ETOH
Bone loss (not a bad as gastric bypass)
Less effective at reversing T2DM compared to bypass

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7
Q

Which bariatric surgery is best at reversing diabtes?

A

Roux-en-Y gastric bypass

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8
Q

Exam findings in PCOS

A

High BMI
High BP
Hyperandrogenism - hirsutism, acne, alopecia
Acanthosis nigricans (Hyperpigmented areas at the nape of neck and axillae)

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9
Q

Pathogenesis of PCOS

A

Poorly understood

Insulin-resistant hyperinsulinemia
LH excess

Both contribute to dysregulation of ovarian steroidogenesis –> hyperandrogenism

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10
Q

Diagnostic criteria of PCOS

A

Diagnosis of exclusion - exclude thyroid disorder, hyperprolactinaemia, Cushing’s, non-classic CAH, androgen secreting tumour, acromegaly

Rotterdam criteria
2 out of 3 of the following:
- Oligo- and/or anovulation
- Clinical and/or biochemical hyperandrogenism
- Polycystic ovaries
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11
Q

Investigations to do in suspected PCOS

A

LH, FSH

  • LH/FSH ratio is raised in PCOS
  • Rule out ovarian failure (high FSH)

Free serum testosterone (high), SHBG (low), free androgen index (testosterone to SHBG ratio)

TSH, prolactin, 17-hydroxyprogesterone, B-HCG, gonadotropin, midnight salivary cortisol (rule out other causes)

Metabolic panel - HbA1c, fasting lipids

+/- pelvic US (will also see if there is outflow obstruction)

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12
Q

Does polycystic ovaries on USS equal PCOS?

A

No

USS features cannot diagnose PCOS alone

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13
Q

Clinical features of PCOS

A

1) Irregular menstrual cycle
- Oligomenorrhoea (menstrual interval >35 days or <8 cycles/year)
- Cycles are usually anovulatory –> heavy bleeding + increased risk of endometrial hyperplasia/ca

2) Hyperandrogenism
- Hirsutism, acne, male-pattern hair loss

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14
Q

How does PCOS increase risk of endometrial hyperplasia/carcinoma?

A

Anovulatory –> unopposed estrogen stimulation –> endometrial hyperplasia/carcinoma

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15
Q

Management of PCOS

Specifically, management for
Hirsutism
Menstrual dysfunction
Infertility
Risk assessment
A

1) Lose weight - 5-10% weight loss can restore ovulation and increase insulin sensitivity in obese anovulatory women
2) Quit smoking

3) Hirsutism
- Combined OCP - suppresses ovarian androgen production, increases SHBG to reduce free androgen
- Spironolactone, cyproterone acetate (block androgen; teratogenic)
- Metformin - insulin-sensitiser, weight loss
- Eflornithine - topical drug that inhibits hair growth

4) Menstrual dysfunction
- COCP or progestin only pill/Mirena (endometrial protection) or cyc`lical progestin (aim 4 bleeds/year for endometrial protection)

5) Infertility
- Lifestyle modifications
- Letrozole (1st line for anovulatory infertility)
- Clomiphene
- Metformin
- Gonadotropin therapy
- IVF

Also
Risk assessment for T2DM, lipids, endometrial ca

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16
Q

What’s primary and secondary amenorrhoea?

A

Primary amenorrhoea

  • Absence of menses, in the presence of normal development of secondary sexual characteristics by age 16
  • Failure of onset of puberty by age 13

Secondary amenorrhoea
- Absence of menstruation for 6 months or more in women with past menses

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17
Q

What’s thelarche?

A

Breast development

Requires estrogen

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18
Q

What’s pubarche?

A

Pubic hair development

Requires androgens

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19
Q

What’s menarche?

A 
First period 
Requires GnRH (hypothalamus), FSH+LH (pituitary), E2+progesterone (ovary), normal outflow tract
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20
Q

How is GnRH released?

A

Pulsatile manner from the hypothalamus

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21
Q

Anosmia and amenorrhoea. What’s the dx?

A

Turner’s

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22
Q

Headache or visual changes and amenorrhoea. What’s the dx?

A

Pituitary mass

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23
Q

Vasomotor symptoms and amenorrhoea. What’s the dx?

A

Primary ovarian failure

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24
Q

What dysmorphic features do you expect in Turner’s?

A

Webbed neck
Short stature
Widely spaced nipples

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25
Q

Causes of amenorrhoea

A

Hypothalamus

  • Gonadotropin deficiency
  • Neoplasm
  • Exercise, weight or nutrition related, chronic illness

Pituitary
- Pituitary adenoma -
macroadenoma, prolactinoma
- Hypopituitarism - post treatment, Sheehan’s

Endocrine

  • Hypothyroidism
  • Hyperprolactinoma including drug induced

Ovarian

  • Gonadal dysgenesis (Turner’s syndrome)
  • Ovarian failure (idiopathic, treatment failure)
  • PCOS

Outflow tract

  • Mullerian agenesis
  • Vaginal atresia
  • Imperforate hymen
  • Asherman syndrome (adhesions within the uterus)
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26
Q

45 XO is…

A

Turner syndrome

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27
Q

List 7 associated conditions in Turner syndrome

A

Coarctation of the aorta

Horseshoe kidney

Autoimmune hypothyroidism

Hearing loss

Metabolic syndrome

Neurocognitive and behavioural issues

Amenorrhoea

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28
Q

What’s primary ovarian insufficiency?

A

Hypergonadotropic hypogonadism <40 years

29
Q

Causes primary ovarian insufficiency

A

Surgery, chemo, radiotherapy
Autoimmune e.g. autoimmune thyroiditis, Addison’s disease, T1DM, MG, hypoparathyroidism
Genetic e.g. fragile X syndrome
Idiopathic

30
Q

How to diagnose primary ovarian insufficiency?

A

BHCG - rule out pregnancy

FSH >40U/L in a two sittings at least 1 month apart OR reduced estradiol and elevated FSH, in the context of amenorrhea and menopausal symptoms

31
Q

Amenorrhoea and FHx of primary ovarian insufficiency, mental retardation, or a tremor/ataxia syndrome.

What is the diagnosis? How do you test for it?

A

Fragile X syndrome

Test for FMR1 premutation -

32
Q

Management primary ovarian insufficiency

A

Counselling

Hormone therapy with cyclical estrogen and progestin to relieve symptoms of estrogen deficiency, maintain bone density, sexual health and QOL. Continue until age of natural menopause (age 50-51).

No therapy to improve fertility

33
Q

Monitoring for primary ovarian insufficiency

A

Annual TSH because of increased risk of developing autoimmune hypothyroidism

Those with positive adrenal ab but normal adrenal function at the initial evaluation (corticotropin stimulation test) should be retested annually

34
Q

What are the cases of hypothalamic amenorrhoea?

A

Stress –> high cortisol
Weight loss –> low leptin
Exercise related

Alters normal pulsatile release of GnRH

35
Q

Initial investigations in amenorrhoea

A 
BHCG
LH
FSH
TSH
E2
Prolactin
Pelvic US
36
Q

Amenorrhoea normal FSH, low E2

DDx

A

?Hyperandrogenism
- Do androgen profile, DHEAS (high in congenital adrenal hyperplasia), 17OHP, Cushing’s screen. Consider adrenal/ovarian imaging

PCOS
Late onset CAH
Cushing’s syndrome
Androgen secreting tumour

37
Q

Leptin

What does it do?

A

Secreted by adipocytes
Acts on the hypothalamus
Long-term control

Leptin deficiency = hyperphagia + impaired satiety = weight gain

38
Q

What if we replace leptin in obesity?

A

As we gain weight, leptin levels go up

Hence leptin replacement doesn’t work for most obesity people = become leptin resistant

39
Q

MC4R

What is it? What does it do?

A

Leptin works on leptin receptor in hypothalamus (arcuate nucleus) –> signals through to MC4R –> reduces appetite

MC4R mutation = obesity

40
Q

Cholecystokinin

What does it do?

A

Satiety factor that regulates meal size
Short-term control

Eat –> stomach stretches –> increased vagal afferents –> brain
Receptors in small intestine –> signal through CCK to the brain

41
Q

Ghrelin
What does it do?
Effects of bypass surgery?

A

Appetite trigger

Produced in small intestine, triggered with food intake

Suppressed after gastric bypass –> less trigger to appetite –> weight loss

42
Q

Brown adipose tissue is defined by

A

Contains uncoupling protein 1 - uncoupling proteins in mitochondria allows expenditure as heat, rather than stored fat.

Amount of brown adipose tissue inversely correlates with BMI, glucose levels

More frequent in women

43
Q

VLCD is ..

When do you do it?

A

<800 calories/day
E.g. optifast

Do this when weight loss is medically urgent
E.g. before surgery

Poor adherence due to hunger after 3-6/12

44
Q

Low calorie diet is …

A

800-1500 calories/day
E.g. Lite n’ easy

Better tolerated for longer than VLCD
Weight loss is slower

45
Q

Moderate calorie reduction is

How much weight loss?

A

About 500 cal less than atypical daily intake

Results in 0.5kg loss /week

46
Q

Orlistat
MOA
Efficacy

A

Blocks gastrointestinal lipase
Blocks absorption of fat

Get fatty diarrhoea if you eat fat

Powerful behavioural tool
But not very effective. Average weight loss 2-3kg over 12 months.

47
Q

Phentermine and topiramate

A

As a combination
Topiramate use is currently off label
Can achieve 12% weight loss in 1 year
But beware of side effects

48
Q

What is the most successful approach to morbid obesity?

A

Bariatric surgery
Most successful weight loss over long term

Mean body weight loss is 25kg

49
Q

Who is eligible for bariatric surgery?

A 
BMI>35 and comorbidities
T2DM
HTN
OSA
Dyslipidaemia
MAFLD
PCOS

Note that TG and HDL may improve but hypercholesterolaemia does not

50
Q

Biliary pancreatic diversion risk of …

A

Cirrhosis

Not done much anymore

51
Q

Risk of bariatric surgery

A 
Mortality
Dehiscence of wound
PE
HAP
Adhesions 
Recurrent hypoglycaemia due to hyperplasia of beta cells (nesidioblastosis)

In general, the safety of gastric bypass is equivalent to knee replacement, and safety of sleeve gastrectomy or banding is same as cholecystectomy

There are issues with safety but properly informed, its extremely useful for morbid obesity

However if you survive short post op period, there is improved mortality long-term

52
Q

Advantages of bariatric surgery

A

Remission of T2DM
Reduced incidence of T2DM
Higher remission and lower incidence rate of HTN and dyslipidaemia
Sustained weight loss

53
Q

Recurrent hypoglycaemia post bariatric surgery

Why?

A

May be mediated by incretin secreted by distal ileum

Increased incretin release –> stimulate beta cells –> beta cell hyperplasia (nesidioblastosis) –> hypoglycaemia

Much higher risk in RYGB

54
Q

GLP1 and PYY … after gastric bypass

How do they work?

A

Increase

GLP1/incretin: secreted upon ingestion of food; reduces glucose by enhancing beta cell insulin secretion, promoting satiety and reducing gastric emptying

Peptide YY: acts within arcuate nucleus to inhibit release of NPY and thereby reduce food intake

55
Q

Dual gastric inhibitory peptide (GIP)/GLP1 receptor agonists = “Twincretins”
What is it?

A

GIP differs from GLP1 in its role of stimulating glucagon secretion during hypoglycaemia; GIP might also promote weight loss by signaling satiety through its receptors present in the hypothalamus

Tirzepatide is a novel once a week dual GIP/GLP1 receptor agonist

56
Q

How is estradiol made in women?

Which 2 cells are involved?

A

2 cells involved

Theca cell
LH binds theca cell
Within theca cell, changes cholesterol to androstenedione –> shuffles to granulosa cells and becomes aromatase

Within granulosa cell
FSH binds to granulosa cells –> aromatase becomes estradiol

57
Q

How is tesosterone and sperm made in men?

Which 2 cells are involved?

A

2 cells involved

Leydig cell
LH binds to leydig cell, changes cholesterol to testosterone

Sertoli cell
FSH binds to sertoli cell –> makes sperm

58
Q

Amenorrhoea
High FSH, low E2
DDx

A

Hypergonadotropic hypogonadism

Do karyotype to look for Turner syndrome (45 XO). If not, then its premature ovarian failure.

59
Q

Amenorrhoea
Low FSH, LH, E2
DDx

A

Hypogonadotropic hypogonadism

Structural
E.g. craniopharyngioma, Kallmann’s syndrome, panhypopituiarism, pituitary adenoma

Functional
E.g. weight loss, exercise, psychological stress

60
Q

Amenorrhoea
Normal FSH, LH, E2
DDx

A

PCOS

61
Q

Turner’s syndrome

Clinical features

A 
45XO
Streak gonads
Dysmorphic features
Short stature
CV abnormalities: coarctation, bicuspid AV, aortic dissection
Renal abnormalities
62
Q

Amenorrhoea and high prolactin

DDx

A

Pituitary tumour (do MRI)

Rarely, hypothyroidism (do TSH)

63
Q

Premature ovarian failure

A

Menopause before age 40
Can have sex chromosome abn e.g. 45X, 47XXY mosaic
Autoimmune polyendocrinopathies
Can be after chemo or radiotherapy

64
Q

How do you estimate ovarian reserve?

A

AMH
Low AMH may indicate low egg reserve
High AMH can occur in PCOS

Can be used as a predictor for IVF success

65
Q

Pathophysiology of PCOS

What’s the role of insulin?

A

Increased pulsed frequency of GnRH –> Increased LH compared to FSH release from anterior pituitary –> increased stimulation of theca cells to produce testosterone, and less oestradiol formation from granulosa cell

Elevated insulin –> promotes androgen formation in theca cell, and hepatic synthesis of SHBG –> increases free testosterone

66
Q

Testosterone deficiency in men

Clinical features

A

Birth: ambiguous genitalia

Puberty: delayed secondary sexual characteristics

Adult: 
Low libido
Erectile dysfunction
Osteoporosis
Infertility
67
Q

What’s primary vs secondary testosterone deficiency in men

A

Primary: inadequate leydig cell function (high LH)
Secondary: pituitary dysfunction (low LH)

68
Q

Klinefelter syndrome

1) Chromosome abn
2) How common?
3) Clinical features

A

XXY

1 in 500 males

Small firm testes
Azoospermia
Increased LH, FSH
Gynaecomastia
Impaired sexual maturation

Endocrinology (9 decks)

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