Biochem of Menopause Flashcards

1
Q

What is the strict definition of menopause?

A

last menstrual period. Functionally we say the last menstrual period is if you haven’t had one in the past 12 months

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2
Q

post-menopause?

A

after last menstrual period

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3
Q

peri-menopause?

A

around the time of last menstrual period

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4
Q

Why are FSH and LH levels so high in menopause?

A

FSH especially high because now we have less negative feedback via estrogen and progesterone on the pituitary and hypothalamus so increasing amounts of FSH and LH are produced. FSH is particularly high because the granulosa cells are even less sensitive to FSH therefore less inhibinB is being made resulting in less inhibition of FSH production at the AP.

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5
Q

What makes estradiol, estriol, and estrone?

A

granulosa cells make estradiol, placenta makes estriol, and adipose makes estrone (a fat person will make more estrone than a skinny one)

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6
Q

What happens to T and E availability and SHBG during menopause?

A

Since testosterone inhibits SHBG production and estrogen stimulates it, but we have less estrogen in menopause, there will be more bioavailability of testosterone to enter the cell (less SHBG so more free T) this can result in increased adrogenic effects like facial hair, hair loss and acne.

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7
Q

Why does growth hormone decrease in menopause?

A

estrogen stimulates GH release and in menopause we have less estrogen (only DHEA being produced by the adrenal gland and being synthesized into estrogen at peripheral tissue like fat cells) so less GH release

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8
Q

Is depressed mood caused by low E?

A

no, but it can be alleviated by low estrogen

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9
Q

Why is osteoporosis more prevalent in women post menopause?

A

Since they have less estrogen, there is less production of OPG which binds RANKL and prevents interaction with RANK therefore preventing activation of osteoclasts. Remember that PTH binds to blasts and causes them to secrete MCSF which binds to clasts and makes them produce RANK. PTH also causes blasts to express RANKL so that they can interact with RANK on coasts and activate them.

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10
Q

How does estrogen inhibit bone resorption?

A

suppress osteoclast activation by inhibiting RANKL, IL-6 and MCSF from osteoblasts. Also increases OPG.

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11
Q

What is fosamax?

A

Bisphosphanate that prevents integrins in osteoclasts from attach to bone matrix so they can’t create an acidic environment for bone resorption.

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12
Q

What are the risks of estrogen therapy?

A

CVD, Breast cancer, risk of clots including stroke, pulmonary embolism and heart attack. If you have a pre-existing condition or are prone to heart disease, then should not take estrogen replacement therapy

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13
Q

How does estrogen depletion affect cardiovascular health?

A

increeases cholesterol levels by increasing LDL and atherosclerotic plaques. Decreases blood flow and causes increased vasoconstriction leading to increased CVD

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