Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology (Semester 6) > 3.1 Gonadal Steroids & inhibitors > Flashcards

3.1 Gonadal Steroids & inhibitors Flashcards

1
Q

_____ stimulates FSH and LH

FSH stimulates _____ cells initiating follicle growth & _____ production

LH acts on _____ cells to stimulate _____ as precursors to oestrogen

LH surge triggers ovulation and follicle conversion to corpus luteum which produces _____

A

GnRH, granulosa, oestrogen, thecal, androgens, progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give 3 general functions of oestrogen and progesterone

A
  1. Feedback
  2. Act on reproductive tract
  3. Act on other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give 3 main drug groups of the repro system

A
  1. Sex Steroids: oestrogens, progestogens, androgens
  2. Inhibitors and Antagonists
  3. Selective oestrogen receptor modulators (SERM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sex steroids are derivatives of _______.

Variations in ring groups lead to changes in what 2 things?

A

cholesterol

Changes in:

  1. function
  2. pharmacokinetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 main sex steroids, how many C’s in their core and give an example of each

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Do progesterone, oestrogen and adrogens act on the same or different receptors?

A

DIFFERENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Steroids are transported bound to ______ (EXCEPT ______) and albumin.

In the liver the sex steroid ______ is almost completly metabolised in one passage through

The metabolites are excreted in urine as ______ and ______

A

SHBG (SHBG = sex hormone-binding globulin), progesterone, progesterone, glucuronides, sulphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does progesterone bind to for transport in the circulation?

A

18% bound to Transcortin
80% bound to serum albumin

Note: does not bind to SHBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Oestrogens contain ______ which bind to nuclear receptors. Once inside the nucleus _______ are activated. This results in a ______ response which differs in different tissues

A

Ligands, transcription factors, pleiotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How many isoforms of the oestrogen, progesterone and androgen receptors are there?

A

oestrogen: 2
androgen: 2
progesterone: 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 3 naturally occuring oestrogens + state which is the main one

A

1) Oestrodiol (main endogenous oestrogen)
2) Oestrone
3) Oestriol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give 5 comparisons of Ethinyloestradiol (synthetic) vs oestradiol (natural)

A

Ethinyloestradiol has:

1) higher oral bioavailability
2) less metabolism in liver and uterus
3) lower binding to hormone carrier protein SHBG
4) 100 fold increased oral potency (lower doses)
5) Less vaginal bleeding but more risk of thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give the most commonly used synthetic oestrogen

+ 2 oestrogen analogues derived from this

A

Ethinyloestradiol

+ Mestranol and Quinestrol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 2 other synthetic oetrogens that are from a non-human source

A

Equilin and Equilenin (from horses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is DES?

A

DES (Diethylstillbestrol) is a synthetic oestrogen which is a non-steroidal oestrogen. This means it is an agonist of the oestrogen receptor but isn’t derived from cholesterol

No longer used due to risk of congenital abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main naturally occuring Progestogen in our body?

A

Progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 2 benefits of progesterone derivatives compared to natural progesterone?

A

Fewer side effects and improved oral bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are Progestins?

A

Progestins are synthetic compounds with progestogen activity.

(Do not necessarily have the 19C core)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Many androgen derivatives are referred to as progestins, why is this?

A

Because although ‘structurally’ these derivatives have a 19C core (androgen) they are able to bind and interact with the progesterone receptor and thus have progestogen activity!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 3 ways in which testosterone can be administed with examples

A

Implants: Testosterone

IM: Enenthate, Proprionate

Oral: Undecanoate, Mesterolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give 2 derivatives of Testosterone or 19-Norandrostane

A

Ethisterone and Dimethisterone

(display progesterone activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give 4 general routes of administration for sex steroids

A
  1. Oral
  2. Transdermal
  3. Implants (subcutaneously or Intrauterine)
  4. Nasal
  5. Vaginal
  6. Intramuscularly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 4 actions and 4 side effects of oestrogen

(Hint: MR BCG is BENT)

A

Actions (MR BCG): Mildly anabolic, Retention of Na+ and H20, ⬇Bone resorption, ⬆Coagulability, Glucose tolerance impaired

S/E (BENT): Breast tenderness, Endometrial hyperplasia, Nausea+vomiting, Thromboembolisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 4 actions and 4 side effects of progesterone

(FAMS AND I)

A

Actions (FAMS): Fluid retention, Anabolic, Mood changes, Secretory endometrium

S/E (AND I): Acne, Nause+vomiting, Depression, Irritability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give 4 actions/side effects of testosterone

(2AAA)

A
  1. Male 2o sex characteristics
  2. Anabolic
  3. Aggression
  4. Acne

+ voice changes and metabolic adverse effects on lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 2 types of OCP?

Incl the effectivness of each

A

1) oestrogen + progestogen (COCP) > 99% effective
2) progestogen only (POP) > 97% effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the role of oestrogen is the COCP? (2)

A

1) Inhibits ovulation by suppressing FSH & LH
2) Alters secretions & cellular structure of endometrial lining to prevent implantation

28
Q

What is the role of progesterone in the COCP and POP? (3)

A

1) Inhibits ovulation by suppressing LH
2) Thickens cervical mucous → impairs sperm movement
3) Alters endometrial lining to prevent implantation

29
Q

Give 4 things we must consider when determing doses of the COCP?

(during clinical trials/ drug formulation)

A

1) dose must be minimum effective dose for whole population (dose > ED100)
2) inter-individual variation eg. body weight, absorption, metabolism and DDIs
3) oestrogen and progestogen doses arrived at empirically (by observation) and then effective o/p ratio is establised
4) reduce dose in trials until irregular bleeding or incidence of pregnancy

30
Q

What are the 4 doses of oestrogens that can be prescribed in the COCP?

A

50, 35, 30, 20mg/day

31
Q

What are the 2 main oestrogens found in the OCP?

A

Ethinyloestradiol and Mestranol

32
Q

What are the 4 generations of Progestogens found in the OCP?

A

1st: norethynodrel
2nd: levonorgestrel, norethisterone
3rd: desogestrel, gestodene, norgestimate
4th: drospirenone (Yasmin: antimineralocorticoid, antiandrogen), norelgestromin (Evra: patch)

33
Q

What is the dosage/cource length is reccomended for the COCP?

A

One tablet daily for 21 days followed by a 7 day pill free period

34
Q

What are the 3 ways in which the COCP can be prescribed?

Define each

A

1) Monophasic: fixed amount of an oestrogen and a progestogen in each active tablet
2) Biphasic/Triphasic: varying amounts of the two hormones according to the stage of the cycle (commonly oestrogen constant progestogen increases)
3) ED (every day): Includes 7 days of placebo tablets

35
Q

How do you decide which formulation of the COCP to prescribe?

A

Depends on patient… Start with Monophasic with the lowest possible risk of side effects (VTE)

If patient experiences spotting consider Biphasic

If patient likes routine/ is forgetful or on multiple medication consider the ED

36
Q

Give an example of a Monophasic pill

A

20-35 micrograms of ethinyloestradiol plus levonorgestrel or norethisterone

37
Q

How is the COCP metabolised

What can therefore be said about its drug-drug interactions?

A

Metabolised by cytochrome P450 (hepatic)

COCP’s efficacy is therefore reduced by enzyme inducing drugs

38
Q

Give 2 drugs that may reduce the efficacy of the COCP?

A

Carbamazepine, phenytoin (enzyme inducing drugs)

39
Q

What should a practitioner refer to when prescribing contraception?

A

UKMEC

40
Q

Give 4 adverse effects of the COCP

A
41
Q

What is the biggest risk factor of the COCP?

A

Breast cancer

42
Q

What is the ‘Mini-pill’ and how is it taken?

What are the 2 formats that can be prescribed?

A

Progestogen-only pill: taken continuously 28 pills – no break

3 or 12 hour formats

43
Q

What is the alternative pill when estrogens are contraindicated

A

Mini-pill / “progestogen-only pill”

44
Q

What is the efficacy of the mini pill dependant on?

A

Efficacy dependent on the care of the user

45
Q

List 4 Progestogens used in the mini pill

A

Levonorgestrel

Norethisterone

Etynodiol diacetate

Desogestrel

46
Q

What is used for Depot provera?

A

Medroxyprogesterone acetate (MPA)

47
Q

What is used for female implants and vaginal rings?

A

Etonogestrel

48
Q

Give the Mode of Action of the mini pill

A

Adverse effect on cervical mucous (thickening)

Adverse effect on the endometrium (structural changes)

Some e.g. desogestrel, prevent ovulation

49
Q

What is the disadvantage of the mini pill?

A

Poor cycle control

Some oestrogen production can lead to irregular bleeding

50
Q

Give 3 options for emergency contraception

(Incl time frames and dosage)

A

1) Up to 72 hrs: Levonorgestrel (levonelle) 1.5mg
2) Up to 120 hrs: Ulipristal acetate (ellaOne) 30mg – progesterone receptor modulator
3) Past 120 hrs: Cu IUD

51
Q

How does the Copper IUD act as an emergency contraceptive?

A

Causes inflammatory reaction in lining of womb

52
Q

Give 2 instances when you would you prescribe HRT?

A

1) In post menopausal experiencing symptoms eg. hot flushes/sweats
2) May or may not be given in women with Osteoporosis

53
Q

What is a contraindication for HRT?

A

Heart disease

54
Q

What is the most common reason to prescribe oestrogen replacement therapy (ERT)

A

After hysterectomy

55
Q

What is the main steroid used in ERT? (incl examples)

A

Oestradiol

e.g. valerate, enanthates, Micronised oestradiol 1-2mg/day, Premarin 0.625-1.25mg/day

56
Q

What is the main steroid used in HRT? + 2 others

A

Medroxyprogesterone acetate (Provera)

Norethisterone

Duphaston

57
Q

What are the 2 types of Combined HRT and explain each

When would you prescribe each?

A

1) Sequential combined: if women is still having some periods within the past year
* Continuous oestrogen given. Progesterone only at the end of each cycle- mimics usual cycle
2) Continuous combined: if patient has had no period in last year
* Constant oestrogen and progesterone

58
Q

Give 4 risks of HRT

A
59
Q

What must you advise all patients of HRT and why?

A

Advise all patients to attend all breast cancer screening due to the Increased risk of breast cancer

60
Q

What is Mifepristone (RU486)?

Incl its MoA and state when it is most commonly used

A

An anti-progestogen!

It is a partial agonist to progesterone receptor which inhibits progesterones action. This sensitises the uterus to prostaglandins (e.g. mesoprostol)

Is used for medical termination of pregnancy, and induction of labour

61
Q

What is Cyproterone acetate?

Incl its MoA and when it is most commonly used

A

An anti-androgen which is a Progesterone derivative

It exhibits a weak progestogenic effect as it is a partial agonist to progesterone receptor. It competes with dihydrotestosterone to bind to androgen receptor

Originally used in combined contraceptive pill (Dianette) BUT now used for acne

62
Q

What is the risk of Cyproterone acetate and therefore what is its course length?

A

Risk of VTE so limited to 3 -18 months

63
Q

What is SERM?

A

Selective oestrogen Receptor Modulators

Exhibits different potencies on different receptor isotypes

64
Q

What is Raloxifene?

Give 3 positives and 1 negatives

A

A SERM

Positives

  • Protects against osteoporosis due to oestrogenic effects on bone, lipid metabolism & blood coagulation
  • Reduces risk of invasive breast cancer in postmenopausal women with osteoporosis
  • No proliferative effects on endometrium & breast

Negatives: Increases hot flushes

65
Q

Which SERMs is commonly used to induce ovulation + its MoA

A

Clomiphene (anti-oestrogen)➞ inhibits oestrogen binding to anterior pituitary which inhibits negative feedback, resulting in increased GnRH and FSH, LH

66
Q

What is Tamoxifen and give 2 common clinical uses

A

Tamoxifen is SERM which is an anti-oestrogen

Primarily used intreatment of ER+ breast cancer and can alos be used to induce ovulation

Pharmacology (Semester 6) (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions