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Endocrinology > Obesity, PCOS, amenorrhoea > Flashcards

Obesity, PCOS, amenorrhoea Flashcards

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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
Causes of amenorrhoea
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)
26
45 XO is...
Turner syndrome
27
List 7 associated conditions in Turner syndrome
Coarctation of the aorta Horseshoe kidney Autoimmune hypothyroidism Hearing loss Metabolic syndrome Neurocognitive and behavioural issues Amenorrhoea
28
What's primary ovarian insufficiency?
Hypergonadotropic hypogonadism <40 years
29
Causes primary ovarian insufficiency
Surgery, chemo, radiotherapy Autoimmune e.g. autoimmune thyroiditis, Addison's disease, T1DM, MG, hypoparathyroidism Genetic e.g. fragile X syndrome Idiopathic
30
How to diagnose primary ovarian insufficiency?
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
Amenorrhoea and FHx of primary ovarian insufficiency, mental retardation, or a tremor/ataxia syndrome. What is the diagnosis? How do you test for it?
Fragile X syndrome Test for FMR1 premutation -
32
Management primary ovarian insufficiency
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
Monitoring for primary ovarian insufficiency
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
What are the cases of hypothalamic amenorrhoea?
Stress --> high cortisol Weight loss --> low leptin Exercise related Alters normal pulsatile release of GnRH
35
Initial investigations in amenorrhoea
``` BHCG LH FSH TSH E2 Prolactin Pelvic US ```
36
Amenorrhoea normal FSH, low E2 | DDx
?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
Leptin | What does it do?
Secreted by adipocytes Acts on the hypothalamus Long-term control Leptin deficiency = hyperphagia + impaired satiety = weight gain
38
What if we replace leptin in obesity?
As we gain weight, leptin levels go up | Hence leptin replacement doesn't work for most obesity people = become leptin resistant
39
MC4R | What is it? What does it do?
Leptin works on leptin receptor in hypothalamus (arcuate nucleus) --> signals through to MC4R --> reduces appetite MC4R mutation = obesity
40
Cholecystokinin | What does it do?
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
Ghrelin What does it do? Effects of bypass surgery?
Appetite trigger Produced in small intestine, triggered with food intake Suppressed after gastric bypass --> less trigger to appetite --> weight loss
42
Brown adipose tissue is defined by
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
VLCD is .. | When do you do it?
<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
Low calorie diet is ...
800-1500 calories/day E.g. Lite n' easy Better tolerated for longer than VLCD Weight loss is slower
45
Moderate calorie reduction is | How much weight loss?
About 500 cal less than atypical daily intake | Results in 0.5kg loss /week
46
Orlistat MOA Efficacy
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
Phentermine and topiramate
As a combination Topiramate use is currently off label Can achieve 12% weight loss in 1 year But beware of side effects
48
What is the most successful approach to morbid obesity?
Bariatric surgery Most successful weight loss over long term Mean body weight loss is 25kg
49
Who is eligible for bariatric surgery?
``` BMI>35 and comorbidities T2DM HTN OSA Dyslipidaemia MAFLD PCOS ``` Note that TG and HDL may improve but hypercholesterolaemia does not
50
Biliary pancreatic diversion risk of ...
Cirrhosis Not done much anymore
51
Risk of bariatric surgery
``` 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
Advantages of bariatric surgery
Remission of T2DM Reduced incidence of T2DM Higher remission and lower incidence rate of HTN and dyslipidaemia Sustained weight loss
53
Recurrent hypoglycaemia post bariatric surgery | Why?
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
GLP1 and PYY ... after gastric bypass | How do they work?
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
Dual gastric inhibitory peptide (GIP)/GLP1 receptor agonists = "Twincretins" What is it?
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
How is estradiol made in women? | Which 2 cells are involved?
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
How is tesosterone and sperm made in men? | Which 2 cells are involved?
2 cells involved Leydig cell LH binds to leydig cell, changes cholesterol to testosterone Sertoli cell FSH binds to sertoli cell --> makes sperm
58
Amenorrhoea High FSH, low E2 DDx
Hypergonadotropic hypogonadism Do karyotype to look for Turner syndrome (45 XO). If not, then its premature ovarian failure.
59
Amenorrhoea Low FSH, LH, E2 DDx
Hypogonadotropic hypogonadism Structural E.g. craniopharyngioma, Kallmann's syndrome, panhypopituiarism, pituitary adenoma Functional E.g. weight loss, exercise, psychological stress
60
Amenorrhoea Normal FSH, LH, E2 DDx
PCOS
61
Turner's syndrome | Clinical features
``` 45XO Streak gonads Dysmorphic features Short stature CV abnormalities: coarctation, bicuspid AV, aortic dissection Renal abnormalities ```
62
Amenorrhoea and high prolactin | DDx
Pituitary tumour (do MRI) Rarely, hypothyroidism (do TSH)
63
Premature ovarian failure
Menopause before age 40 Can have sex chromosome abn e.g. 45X, 47XXY mosaic Autoimmune polyendocrinopathies Can be after chemo or radiotherapy
64
How do you estimate ovarian reserve?
AMH Low AMH may indicate low egg reserve High AMH can occur in PCOS Can be used as a predictor for IVF success
65
Pathophysiology of PCOS | What's the role of insulin?
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
Testosterone deficiency in men | Clinical features
Birth: ambiguous genitalia Puberty: delayed secondary sexual characteristics ``` Adult: Low libido Erectile dysfunction Osteoporosis Infertility ```
67
What's primary vs secondary testosterone deficiency in men
Primary: inadequate leydig cell function (high LH) Secondary: pituitary dysfunction (low LH)
68
Klinefelter syndrome 1) Chromosome abn 2) How common? 3) Clinical features
XXY 1 in 500 males ``` Small firm testes Azoospermia Increased LH, FSH Gynaecomastia Impaired sexual maturation ```

Endocrinology (9 decks)

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