Brainscape's Knowledge GenomeTM

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


See full index

IPFC 1 Final > Female hormones Pharmacology > Flashcards

Female hormones Pharmacology Flashcards

1
Q

What is the precursor for all steroid hormones

A

Cholesterol

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

What are the 3 types of estrogen. What is the main source of estrogen pre-menopause and post-menopause? where?

A
  • Estradiol (pre-menopause, ovary)
  • Estrone (post-menopause, adipose)
  • Estriol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is Progesterone made

A
  • Ovaries
  • testes
  • Adrenal
  • Placenta
  • Cholesterol
  • Corpus luteum (ovary in the 2nd half of menstrual cycle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which part of the hormonal cycle does progesterone and estrogen get released?

A

LH and FSH relaese produces estrogen and progesterone

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

Where is Estrogen receptor Alpha ER-a found?

A
  • Female reproductive tract
  • Mammary gland
  • Hypothalamus
  • Endothelial cells
  • Vascular smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is ER-B found

A

Ovaries
(and in lower levels in lung, brain, bones, vasculature)

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

How do estrogen receptors work?

A
  1. Estrogen receptor agonist (ex. estradiol) enters cell –> Binds ER
  2. ER dissociates from heat shock proteins –> forms
    - homodimer: ER-a/ER-a or heterodimer ER-a/ER-B
  3. ER dimers binds to estrogen response
  4. Recruitment of co-activators –> gene transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Can estrogens bind GPCRs? what is its effect?

A

Yes
- Cause faster, non-genomic estrogenic activity

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

Differentiate between PR-A and PR-B

A

Both have identical ligand binding

PR- A
- inhibits actions of PR-B (recruiting co-REPRESSORS)
- missing first 165 N-terminal amino acids of PR-B

PR-B
- Stimulates progesterone activity (by recruitment of co-ACTIVATORS)

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

How do progesterone receptors work?

A
  1. PRs are found in nucleus, in an inactive state, bound to heat shock proteins
  2. Progesterone receptor agonist enter nucleus –> binds to PR
  3. Binding causes dissociation of heat shock proteins
  4. Receptor dimers form –> bind to progesterone response elements on target genes
    (makes homodimers or heterodimers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the physiological effects of estrogen (5)

A
  • Causes endometrial proliferation
  • Increases water in cervical mucous (easier for sperm to get in)
  • Inc differentiation of osteoblasts, Reduces osteoclast activity (= good bones)
  • Changes in lipid levels
  • Changes in blood clotting factor levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the physiological effects of progesterone (4)

A
  • Inhibits endometrial proliferation caused by estrogen (matures endometrial cells instead )
  • Makes cervical mucous thicker (opposite of estrogen)
  • Maintains pregnancy
  • Decline in progesterone at the end of cycle causes menstruation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain what the other ovarian hormones do:
Androgens
Inhibin
Activin
Relaxin

A

Androgens
- small amounts of testosterone are produced

Inhibin
- inhibits FSH production

Activin:
- promotes FSH release

Relaxin:
- Released in response to LH

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

What is the MOA of progesterone receptor antagonists. Give examples.

A

Bind and block progesterone receptors

Mifepristone (terminate pregnancy)
Ulipristal (partial antagonist)

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

What is the MOA of estrogen receptor antagonist. Give examples

A

Bind to estrogen receptors and cause dimerization + DNA binding (like estrogen)
- then recruit co-receptors –> inhibit gene transcription

Ex.
- Clomiphene
- Fulvestrant

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

Differentiate between Estrogen receptor antagonists vs agonists. Protein enzyme activity? relax/tighten chromatin?

A

Agonists (co-activators)
- Histone acetyltransferase activity
- Relax chromatin –> allow transcription

Antagonists (co-repressors)
- Histone deacetylase activity
- Tighten chromatin –> inhibit transcription

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

Explain how selective estrogen response modulators work (SERMs)

A

Alter the conformation of ER-a and/or ER-B
- unique to SERMs
- lead to different interactions with co-activators/co-repressors
- either partially estrogenic, no activity, or anti-estrogenic activity

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

Give examples of SERMs (2) explain them

A
  1. Tamoxifen: breast cancer
    - also maintains bones
  2. Raloxifene: Osteoporosis
    - anti-estrogenic activity in breasts (reduce growing)
    - estrogenic activity in bone (anti-resorptive; doesn’t break down)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain indirect-acting agents
Give example of an irreversible & reversible inhibitor?

A

Aromatase inhibitors used to block estrogen production
- used for breast cancer
- No positive effect on bone (like tamoxifen)
- Used as an add-on/second line to tamoxifen treatment

Irreversible: Exemestane (Aromasin)
Reversible: Anastrazole (Arimidex), Letrozole (Femara)

20
Q

What are other compounds that have estrogenic activity

A

Plant-based compounds:
Soy isoflavones (used to manage menopausal symptoms)

Synthetic agents:
- Bisphenol A

21
Q

What are the different types of hormonal contraceptives available?

A
  1. Estrogen/progestin combinations (COCs)
    a. Fixed dose: every dose contrains the same ratio
    b. Phasic: dose of each hormone varies depending on stage of cycle
  2. Progestin-only formulations
22
Q

What hormones do COCs contain?

A

Estrogen (ethinyl estradiol)
Progestin
ex. Desogestrel (less androgenic activity)
ex. Drospirenone (mineralocorticoid receptor antagonist)

23
Q

What is the purpose of administering COCs for 21 days of 28 day cycle

A

Reduce exposure to hormones, but retain enough activity to maximize anti-ovulation effects
- Also to reduce breakthrough bleeding

24
Q

What is the primary and secondary MOA of COCs

A

Primary
- The estrogen inhibits FSH secretion (inhibit follicular development)
- Progestin to inhibit LH secretion (inhibit LH surge and ovulation)

Secondary
- Progestin to alter cervical mucous (inhibit sperm passage)
- estrogen/progestin alter endometrium (decrease chance of implantation)

25
Q

What is the MOA of progestin-only contraceptives (3)

A
  • Change cervical mucous –> inhibit fertilzation/sperm passage
  • Change endometrial lining –> inhibit implantation
  • Inhibit LH surge –> prevent ovulation
26
Q

What are examples of progestin-only contraceptives

A
  • Minipill (oral)
  • depot medroxyprogesterone (IM)
  • subdermal implants
  • Intrauterine device (releases levonorgesterol, localizes the progestin levels)
27
Q

Explain what clomiphene citrate is for? What class?

A

Estrogen receptor antagonist
- used to treat anovulation
(fertility enhancer)

28
Q

What is the MOA of clomiphene citrate

A

inhibits the negative feedback of estrogen at hypothalamus and pituitary
- Tricks pituitary into thinking estrogen is low –> releases more estrogen
- Inc in FSH to promote maturation and release of follicle

**Use in beginning of cycle, day 2-5

29
Q

What cons can clomiphene citrate cause? ADRs?

A

Cons
- increase chance of twins (multiple follicles releasing at once)
- Inhibits estrogen action at endometrium which makes it non-optimal for fertilization and implantation

ADRs
- Ovarion cysts
- Hot flashes
- Headaches
- Blurred vision

30
Q

What is the MOA of Gonadotropins

A

Used to induce ovulation

  1. Daily injection of exogenous FSH –> until 1-2 mature follicles develop
  2. Injection of hCG –> completes follicle maturation + induces ovulation
  3. Attempt fertilization (sex or insemination)
31
Q

What can folate deficiencies result from?

A
  • Chronic malnutrition
  • Alcohol use
  • Vit C deficiency
  • Chronic liver disease
  • Malabsorption
32
Q

Why is folic acid supplement required?

A

Required for
- purine/thymidine biosyntehsis
- DNA methylation
- other metabolic reactions

33
Q

Differentiate between purine and thymidine reactions

A

Purine reaction: folic acid is regenerated
Thymidine reaction: folic acid is NOT regenerated

34
Q

Which antihistamines are used in N/V in pregnancy? (3)

A

Doxylamine: H1 antagonist with anti-emetic effects
- Also used dimenhydrinate, diphenhydramine
- First gen AHS cause sedation –> can be used as sleep-aid in pregnancy

Diclectin: Doxylamine + Pyridoxone (vit B6)
- anti-nausea effects

Promethazine: pehnothiazine antihistamine
- For morning sickness
- + metoclopramide treats nausea associated with opioid admnistration during labour

35
Q

What antipsychotic is used in N/V for pregnancy? What cautions should you take with this?

A

Chlorpromazine
- D2 antagonist at the CTZ _ some antihistaminic/anticholinergic activity
- treats morning sickness and during labour to promote analgesia and amnesia

Cautions
- Do not use during near-term (risk of maternal hypertension
- Use low doses and not chronically

36
Q

What are the promotility agents used in N/V for pregnancy? MOA?

A

Metoclopramide, domperidone:
- block dopamine D2 receptors
- Enhance gastric emptying (without affecting intestinal motility)

37
Q

What are ADRs of metoclopramide, domperidone, and both?

A

Both
- increased prolactin –> galacttorrhea, menstrual disturbances

Metoclopramide
- Extrapyramidal effects
- Drowsiness, insomnia, anxiety, agitation

domperidone
- rare neuropsychiatric effects (does not cross BBB)

38
Q

What is the MOA of 5-HT3 Antagonists?
Primary and secondary

A

Primary: block 5-HT3 receptors on vagal/spinal afferent nerves from GI tract

Secondary: block centra 5-HT3 receptors in vomiting center/chemoreceptor trigger zone

** no effect on muscarinic receptors/ gastric motility

39
Q

What is used in emergency contraceptives? Primary MOA?

A

Levonorgestrel (progestin) but in high doses
- to prevent ovulation and to impede sperm by increasing cervical mucous viscosity

40
Q

What do Yuzpe regimens include in emergency contraceptives?

A

Includes both progestins and estrogens
- in addition to progestin effects, the estrogen may also interfere with implantation of a fertilized egg

41
Q

What is the MOA of mifepristone ? Used with what?

A

Blocks progesterone receptors
- causes thinning of endometrium, cervical ripening/dilation

Used with PGE1 or misoprostol
- induce uterine smooth muscle contractions

42
Q

Examples of Prostaglandins and MOA. other uses of it?

A

Misoprostol
- causes cervical ripening/dilation

Other uses:
- induce labour
- medical abortion
- post-miscarriage treatment

43
Q
A
44
Q

What is oxytocin used for?

A

Increase uterine contractions during labour

45
Q

When is methotrexate used? what is the MOA

A

Used in ectopic pregnancy
- inhibits rapidly dividing tissue, disrupts folic acid productions (slows cell division)

46
Q

What are tocolytics used for? MOA

A

Prevents labour
- induce uterine smooth muscle RELAXATION

IPFC 1 Final (13 decks)

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