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GGE > Gametes - PCOS Case > Flashcards

Gametes - PCOS Case Flashcards

1
Q

HEADDSS

A

Home

Education

Activities

Drugs

Diet

Sex

Suicide

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2
Q

CAH =

A

Congenital adrenal hyperplasia

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3
Q

Female Athlete Triad

A

hypothalamic amenorrhea

high level of intensity of exercise reduces body fat to a level so low that menstruation could be affected

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4
Q

aldosterone, cortisol, tesotosterone and estradiol production

A
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5
Q

what happens if someone is lacking the enzyme 21-OH

A

cannot produce aldosterone, cannot produce cortisol

-ve feedback on anterior pituitary to stop it overproducing ACTH

No -ve feedback so lots of ACTH

ACTH present, DHEA can still be produced as well as testosterone

CAH

No 21-OH enzyme, don’t produce cortisol but will overproduce adrenal androgens

Not enough cortisol -> hypoglycaemia

weak and dizzy between meals (cortisol maintains blood glucose levels) ⇒ muscle wastage

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6
Q

Pathophysiology of PCOS

A

metabolic and reproductive endocrine disorder

most common cause of female infertility

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7
Q

causes of PCOS

A

obesity

excess of ovarian androgen production

hyperinsulinemia (T2D)

intrauterine environment

genetic factors

hypothalamic-pituitary-ovarian axis

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8
Q

how might PCOS present

A

Excess insulin - both androgens and oestrogen, stimulates keratinocytes to hyper divide - increased proliferation

Insulin and IGF-1 linked to this increase in keratinocyte proliferation

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9
Q

genetic studies of PCOS

A

increased prevalence of PCOS related traits in siblings with indications for an autosomal dominant model of inheritance

prevalence - 51-66% in 1st degree relatives

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10
Q

genes associated with increased risk of PCOS

A

CYP11a

HSD17B5

D19S884

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11
Q

CYP11a

A

cholesterol - pregnenalone

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12
Q

HSD17B5

A

androstenedione - testosterone

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13
Q

D19S884

A

PCOS susceptibility locus - associated with insulin resistance

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14
Q

INSR

A

insulin receptor has been validated as a risk locus for PCOS

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15
Q

intrauterine environment and PCOS

A

2nd trimester amniotic fluid testosterone levels are elevated in female foetuses of PCOS vs normal mothers

the apparent of IU milieu in poorly controlled diabetics who end with stillborn foetuses showed ovarian changes similar to those seen in PCOS

link between androgen excess in utero and the maternal environment remains unclear

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16
Q

disorders of HPO axis

A

Increased GnRH vfrom hypothalamus

excessive LH secretion relative to FSH by pituitary gland

LH stimulates ovarian thecal cells to produce Xs androgen (Granulosa cells also produce inhibin - FSH goes up, inhibin works to stop anymore but we don’t have the same mechanism for LH so it continues to form)

ineffective suppression of LH pulse frequency by estradiol and progesterone

andorgen excess increases LH by blocking hypothalamic inhibitory feedback of progesterone

17
Q

Kisspeptin

A

a hypothalamic peptide coded by the Kiss1 gene

novel neuromodulator that acts upstream of GnRH

sensitive to sex steroid feedback and metabolic cues

recognised as a crucial regulator of the onset of puberty, the regulation of sex hormone mediated secretion of gonadotrophins and the control of fertility

18
Q

insulin resistance and PCOS

A

common feature

occurs in both obese and non-obese PCOS women

anomalies in insulin receptor mediated transduction

obesity has synergystic effect on glucose metabolism and IR

19
Q

criteria for IR syndrome

20
Q

relationship between insulin and androgens

A

ALTERED INSULIN

HYPERLIPIDAEMIA

ALTERED HPO

21
Q

effect of increased insulin levels

A

increased insulin levels can stimulate androgen production

insulin can stimulate adrenal steroidogenesis by enhancing sensitivity to adrenocorticotrophic hormone and increasing pituitary LH release

insulin lowering therapies can restore menstrual cycles in some anovulatory women with PCOS

defects in insulin receptors have been found in up to 1/2 of women with PCOS

22
Q

PCOS - lipid profiles and obesity

A

obesity has high prevalence in PCOS cases

70% of patients with PCOS have an abnormal lipid profile

  • high TGs
  • low HDL cholesterol
23
Q

pathways leading to androgen excess in PCOS

24
Q

morphology of polycystic ovary

A

12+ follicles measuring 2-9mm in diameter and/or increased ovarian volume (> 10 cm3)

follicles are usually PERIPHERAL in location

25
Q

long term consequences of PCOS

A

increased risk of diabetes

increased risk of CV disease

Increased risk of carcinoma

26
Q

PCOS and CV risk factors

A

dyslipidemia

raised triglycerides

elevation of LDL

reduced HDL

raised small dense LDL-III

increased hepatic lipase activity

elevated plasminogen activator inhibitor, PAL-1

(consequences of androgens or hyperinsulinemia)

27
Q

PCOS and cancer

A

increased risk of endometrial cancer

GGE (33 decks)

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