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Clinical Pharmacology & Intro to Prescribing > Session 4: Reproductive and Post-reproductive Health > Flashcards

Session 4: Reproductive and Post-reproductive Health Flashcards

1
Q

What are sex steroids synthesised from?

A

Cholesterol

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2
Q

Briefly explain the sex steroid synthesis.

A

Cholesterol -> pregnenolone -> progesterone -> testosterone -> estradiol.

CYP17 turns progesterone into testosterone.

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3
Q

Explain the properties of the steroid hormone receptor.

A

Classic nuclear receptor that exert effects through gene transcription.

It is also a membrane receptor for oestrogen.

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4
Q

Major effects of oestradiol

A

Stimulates growth of the endometrium and breast.

It also stimulates production of progesterone receptors.

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5
Q

Major effects of progesterone.

A

Stimulates growth of the endometrium and brest.

Maintains pregnancy

Also inhibits production of oestrogen receptors.

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6
Q

Major effects of testosterone

A

Stimulates male characteristics

Hairy body

Deep voice

Anabolism

Aggression

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7
Q

Other oestrogen actions.

A

Mildly anabolic

Sodium and water retention

Raises HDL and lowers LDL

Decrase bone resportion

Impair glucose tolerance

Increase blood coagulability

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8
Q

Side effects of oestrogen.

A

Breast tenderness

Nausea and vomiting

Water retention

Increased blood coagulability

Thromboembolism

Impaired glucose toelrance

Endometrial hyperplasia and cancer

Ovarian metaplasia and cancer

Breast hyperplasia and cancer

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9
Q

Other progesterone actions.

A

Secretory endometrium

Anabolic effects

Increases bone mineral density

Fluid retention

Mood changes

Maintains pregnancy

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10
Q

Side effects of progesterone

A

Weight gain

Fluid retention

Anabolic

Acne

Nausea

Vomiting

Irritability

Depression

PMS

Lack of concentration

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11
Q

Actions and side effects of testosterone.

A

Male secondary sex characteristics

Anabolic

Acne

Voice changes

Increased aggression

Increased risk of atherosclerotic disease in males due to the HDL-C/LDL-C ratio being lower.

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12
Q

Where is oestrogen absorbed?

A

Natural and synthetic oestrogens well absorbed in the GI tract and also readily absorbed from skin and mucous membranes.

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13
Q

Where is oestrogen metabolised?

A

Liver

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14
Q

Where is oestrogen excreted?

A

In the urine as glucuronides and sulfates.

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15
Q

Explain the pharmacokinetics of progesterone.

A

Injected progesterone is bound to albumin with some stored in adipose tissue.

Metabolised in the liver and then excreted in the urine conjugated to glucuronic acid.

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16
Q

Adverse effects of the COCP.

A

Risk of thromboembolism which is however usually small but severely increased with smoking.

More commonly associated with other risk factors such as obesity and hypertension.

17
Q

Where are COCP and POP contraceptives metabolised?

A

In the liver by CYP 450 enzymes.

18
Q

Give examples of drugs that reduce oral contraceptive efficacy and why.

A

Anti-epileptics like carbamazepine or phenytoin.

Antibiotics such as rifampicin and rifabutin.

Some natural products such as St John’s Wort.

These all cause an increase in the production of hepatic CYP450.

19
Q

Explain the interaction between soya protein and oestrogen.

A

Enhance oestrogen absorption and reduce its storage in adipose and muscle.

This menas that the half-life is reduced from 15 hours to 7 hours.

20
Q

Why is HRT prescribed?

A

To deal with the peri-menopausal, menopausal and post-menopausal effects.

For symptoms such as hot flushes/sweats and dyspareunia.

Osteoporosis

However no effect on heart disease.

21
Q

Give examples of steroids used in HRT.

A

Oestradiol such as valerate, enanthate, micronised oestradiol, ethinyl estradiol.

Premarin

Provera

Norethisterone

Levonorgestrel

22
Q

Routes of administration of HRT.

A

Oral

Transdermal

Implant

Transvaginal

Nasal

23
Q

Should HRT be given in prevention of heart disease?

A

No it is not effective for it and should not be prescribed for it.

24
Q

Risks of HRT.

A

Unopposed oestrogen leading to increased risk of developing endometrial and ovarian cancers.

Opposed oestrogen increases risk of developing breast cancer.

Increased risk of venous thromboembolism.

Increased risk of stroke

25
Q

How does HRT cause an increased risk of venous thromboembolism?

A

Increased activated protein C resistance.

Increased thrombin activation

Decreased anti-thrombin III activity

Decreased protein S levels

Decreased Factor VII levels

Decreased Tissue factor pathway inhibitor

26
Q

How can HRT be beneficial for cardiovascular disease?

A

Increased HDL-C

Decreased oxoLDL-C

Decreased TAG

Decreased lipoprotein A

This will however not have any effect if the patient is already overweight

27
Q

What type of HRT is associated with stroke?

A

Use of oral but not transdermal oestrogen.

28
Q

What is Mifepristone?

A

Progesterone and glucocorticoid receptor antagonist

29
Q

Action and use of mifepristone.

A

Acts as an anti-progesterone which sensitise the myometrium to prostagland-induced contractions in order to terminate pregnancy.

30
Q

What is a SERM?

A

Selective Estrogen Receptor Modulator

Can be either pure agonists or pure antagonists.

31
Q

Give examples of SERMs.

A

Tamoxifen

Raloxifene

Clomiphene

32
Q

Action of clomiphene and its use.

A

Treatment of anovulation.

Competes with the oestrogen for oestrogen receptor binding.

This leads to anovulation induction through increased production of anterior pituitary hormones.

33
Q

Features of tamoxifen.

A

A pro-drug with little affinity to oestrogen receptors but as it is metabolised in the liver to an active derivate it will start to compete with oestrogen for binding to oestrogen receptors.

34
Q

Action and use of tamoxifen.

A

In endometrium it acts as an ER agonist.

In breast it acts as an ER antagonist.

This means that in endometrium it will cause hyperplasia and can cause endometrial cancer as well.

In breast it binds to the ER and causes cells to arrest the cell cycle and works as protective against breast cancer.

35
Q

What is ulipristal acetate?

A

A selective progesterone receptor modulator.

36
Q

Use of ulipristal acetate.

A

Emergency contraception.

Primary mode of action is thought most likely to be delay or inhibition of ovulation.

It is also effective for the treatment of uterine fibroids.

Clinical Pharmacology & Intro to Prescribing (24 decks)

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