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week 1 lec 3 Flashcards

1
Q

PCOS is characterized by (3)

A

irregular menstrual periods
high androgen levels
polycystic ovaries

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2
Q

most common endocrine disorder in reproductive age people with uterus/ovaries

A

PCOS

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3
Q

3 hormonal imbalances in PCOS

A

inappropriate gonadotropin secretion
insulin resistance with hyperinsulinemia
excessive androgen production

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4
Q

wk 1 lec 3 pathophysiology chart of PCOS on page 6 and slide 10

A

:)

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4
Q

causes of PCOS?

A

unknown but… genetic, environment and fetal exposure to high androgen levels

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5
Q

LH to FSH ratio is PCOS

A

increased

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6
Q

GnRH in PCOS

A

increased pulsatile release

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7
Q

progesterone and estrogen and androgens in PCOS

A

anovulation causes decreased progesterone release and increased estrogen

increased androgens

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8
Q

acanthuses ingrains in PCOS

A

from insulin resistance

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9
Q

hirsutism, acne, alopecia in PCOS from

A

androgen excess

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10
Q

altered GnRH pulsaility leads to increase ___ compared to ___

A

LH increases (increase pulse frequency and amplitude)

compared to FSH (remains the same)

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11
Q

FSH vs LH function

A

FSH- stimulates growth of ovarian follicles

LH- stimulates ovulation and ovarian hormone production (i.e. stimulates androgen production)

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12
Q

LH to FSH ration in PCOS

A

above 2:1

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13
Q

lower FSH in PCOS leads to

A

reduction in aromatase activity, less conversion of testosterone to estrogen in the granulosa cells

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14
Q

dominant follicles in PCOS?

A

dominant follicle doesnt develop bc LH secretion occurs before it can

so theres several immature follicles (difficult to ovulate)

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15
Q

which phase is missing since no ovulation in PCOS

effect on hormones

A

no luteal phase

no progesterone, leaving estrogen unopposed –> endometrial neoplasia risk

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16
Q

increased LH leads to

A

increased steroid hormone proaction in ovary –> excess androgen production

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17
Q

high androgen levels cause

A

dyslipidemia, hirsutism, acne

peripherally converted into estrongen in adipose tissue (augmented in obese people)

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18
Q

androgens turn into what peripherally

A

estrogen (in adipose tissue)

cause high estrogen levels all cycle (no longer fluctuate) and impacts feedback loop at hypothalamus and pituitary

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19
Q

risk of endometrial hyperplasia in PCOS

A

from chronically elevated estrogen stimulating endometrial cells

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20
Q

follicular atresia from

A

insulin resistance and hypersecretion

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21
Q

diabetes and PCOS

A

from insulin resistance and hypersecretion and elevated blood glucose

compensatory hyperisulinemia

reduced glucose uptake from target cells in response to insulin

insulin resistance in both lean and obese PCOS patients

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22
Q

insulin stimulates what from the pituitary

A

LH and FSH

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23
Q

insulin increases release of what from theca cells

A

androgens

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24
insulin decreases production of what in the liver
Decreases the production of SHBG in the liver→increased circulating androgens
25
androgens get stimulated by 2 things
elevated LH and insulin
26
where are androgens mainly produced
ovarian theca cells (testosterone and androstenedione)
27
elevated male hormones in PCOS
free testosterone and DHEAS
28
sex hormone binding globulin (SHBG) is made
in the liver
29
SHBG production is suppressed by
insulin production
30
less circulating SHBG causes what effect on androgens
more androgens are unbound and free to circulate and bind with end-organ receptors (hair follicles, sebaceous glands→acne)→clinical hyperandrogenism
31
anovulation from many things...
-altered GnRH pulsailty -insulin resistance (i.e. metformin helps with oligo-ovulation) -androgens produced by large # of astral follicles
32
short term vs long term consequences of PCOS and hyperandrogenism
short term: obesity, infertility, sleep apnea, irregular menses, anxiety, depression, abnormal lipid levels, ANFLD, hirsutism/acne/androgen alopecia, insulin resistance/ acathosis nigricans long term: T2DM, endometrial cancer, cardiovascular disease
33
obesity and PCOS`
insulin resistance etc
34
PCOS and infertility
from anovulatory cycles
35
menstural dysfunction in PCOS
amenorrhea, oligomenorrhea and heavy bleeds (lead to iron deficiency)
36
result of anovulation
lack of progesterone production
37
chronic estronge exposure (that unopposed by progesterone) leads to
chronic exposure of the endometrium→instability of thickened endometrium can lead to unpredictable bleeding
38
oligomenorrhea vs amenorrhea
Oligomenorrhea (less than 9 menstrual periods in a year) and amenorrhea (absence of menses for 3 or more months) usually begins with menarche in people with PCOS
39
what menstural intervals warrant further investigation
<20 or >45 days > 2 years after menarche or an interval >90 days at any time
40
aging and PCOS and menstural dysfunction
As people with PCOS age, regular cycles may resume (due to lower antral follicle count, and decrease in follicular androgen production)
41
obstructive sleep apnea
PCOS and obesity
42
dyslipidemia and PCOS
high LDL and triglyceride lower HDL high cholesteroll: HDL ratio --> CVD
43
3 parts of hyperandrogenism
hirsutism acne alopecia
44
what signs of rapid increase in androgens are not related to PCOS and should be investigated to see if have androgen secreting tumor
increased muscle mass, deepening voice, and cliteromegaly
45
hirsutism- what causes the hair follicle changes
in the hair follicle testosterone is converted by 5 alpha reductase to DHT (dihydrotestosterone) testosterone and DHT convert short vellus hair to terminal hair (DHT is more effective) [[permanent and irreversible]]
46
what turns testosterone into dihydrotestosterone in hair follicle
5 alpha reductase
47
most common areas of hirsutism (androgen sensitive areas)
upper lip, chin, sideburns, chest, and linea alba of the lower abdomen
48
racial impacts on hirsutism
Mediterranean individuals have a greater concentration than Northern Europeans, and a much higher concentration than Asians.
49
alopecia (less common) in PCOS is caused by
excessive 5 alpha reductase activity in hair follicle --> increase DHT levels terminal hairs that aren't dependent on androgens transform to a vellus hair follicle- leading to alopecia
50
alopecia in PCOS
In certain hair-bearing areas, androgens activate sebaceous glands and transform vellus follicles (A) into terminal follicles (B), causing hirsutism. Conversely, under androgen influence, terminal hairs that were previously not androgen-dependent (C) shrink and revert to vellus-like hairs, leading to balding (D).
51
4 factors involved in pathogensis of acne
1. Blockage of the follicular opening by hyperkeratosis 2. Sebum overproduction 3. Proliferation of commensal bacteria (Propionibacterium acnes) 4. Inflammation
52
what causes an increase in sebum formation which leads to inflammation and comedones formation and scarring [acne]
testosterone --> DHT in sebaceous gland
53
treat acne in PCOS
* Minimizing inflammation * decreasing keratin production * lowering colonization of P. acnes (bacteria) * reducing androgen levels to diminish sebum production
54
acanthuses nigricans and insulin resistance and hyperinsulinemia can lead to
keratinocyte growth
55
impaired glucose tolerance metrics
fasting glucose of 6.1-6.9 mmol/L or Hb A1c of 6.0-6.4% or 2 hour post oral glucose tolerance test with 75 grams of glucose 7.8-11 mmol/L
56
what further increases degree of insulin resistance in PCOS
anovulation
57
how to test for impaired glucose tolerance (IGT) and T2DM
75 grams oral glucose tolerance test fasting and 2 hour post glucose load OR HbA1c too...
58
recommend oral glucose tolerance test for T2DM and impaired glucose tolerance if
high-risk women BMI > 25 kg/m2 or BMI > 23 kg/m2 in Asian women, history of abnormal glucose tolerance or family history of diabetes, hypertension, or high risk ethnicity and those planning pregnancy or seeking fertility treatment.
59
endometrial neoplasia/cancer
mitogenic changes increase with involution and unopposed estrogen
60
endometrial neoplasia from
hyperandrogenism, hyperinsulinemia and obesity decrease circulating SHBG and increase circulating estrogen
61
develop endometrial neoplasia if
>40 yrs old obese and chronic anovulation
62
metabolic syndrome 4 characteristics
insulin resistance, obesity, dyslipidemia, and hypertension.
63
pregnancy and PCOS
miscarriage, gestational diabetes, hypertesnion, preterm birth esp if obese
64
how do increased use of fertility intervention in those with PCOS cause an increased risk of
multi-fetal gestations risk increases→increases risk of maternal and neonatal complications
65
cutaneous marker of insulin resistance
acanthuses nigricans
66
where is acathosis nigricans
A thick grey-brown velvety plaque in flexure areas such as back of neck, axillae, waist, groin, infra-mammary crease (below the breast).
67

BMS250 (52 decks)

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