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2402 supp > 2402 REPRO(F) > Flashcards

2402 REPRO(F) Flashcards

1
Q

GnRH

Gonadotropin Releasing Hormone

A

Produced in the hypothalamus

Stimulates FSH and LH secretion by the anterior pituitary gland.

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2
Q

FSH

Follicle Stimulating Hormone

A

Produced in the anterior pituitary

Stimulates
follicle recruitment and maturation in the ovaries.

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3
Q

LH

Luteinising Hormone

A

Produced in the anterior pituitary

Stimulates release
of the ovum from the mature ‘graafian’ follicle and conversion of the remaining follicle into
the corpus luteum structure.

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4
Q

Estrogen – The major female hormone.

A

Mostly produced by the ovaries and has a
negative feedback effect on GnRH, LH and FSH secretion

High levels of estrogen reduce GnRH and MAINLY FSH secretion, except during mid cycle-ovulation

–> Estrogen
negative feedback flips to estrogen positive feedback AND high levels of estrogen increase
GnRH and FSH secretion

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5
Q

Progesterone

A

Building up the endometrium to allow implantation of a

fertilised ovum.

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6
Q

High levels of progesterone induce…

A

A negative feedback effect on the

hypothalamus to reduce GnRH secretion and MAINLY LH secretion (to prevent ovulation).

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7
Q

Inhibin

A

A hormone that INHIBITS only FSH secretion

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8
Q

Describe the HPO axis:

A
  1. GnRH neurons reside in the hypothalamus
  2. Neurons have terminal projections in the median eminence
  3. GnRH is released from the nerve terminals in the ME
  4. GnRH travels through the hypothalamic-hypophyseal portal
    (blood) system to the anterior pituitary
  5. GnRH stimulates LH and FSH production by gonadotroph
    cells in the AP
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9
Q

The Menstrual Cycle consists of 2 phases:

A

Follicular

Luteal

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10
Q

The Follicular Phase:

A 
1. Low levels of oestrogen
stimulate FSH release (-ve
feedback)
2. FSH stimulates the recruitment
of many ‘primary’ follicles.
3. Only the most dominant
oestrogen secretor develops into
the Graafian follicle (contains the
ovum)
4. Secondary and mature follicles
increase plasma oestrogen
5. High plasma oestrogen mid-cycle
stimulates LH release (+ve
feedback)
6. LH causes the Graafian follicle to
rupture and release the ovum
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11
Q

The Luteal Phase:

A 
1. The ruptured follicle becomes
the corpus luteum which
secretes progesterone and
oestrogen
2. If the ovum is not fertilised,
progesterone and oestrogen
secretion stops and the
endometrium sheds
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12
Q

Menopause:

A
  1. Cessation of menstruation (~50 yo)
  2. Run out of follicles (sort of)
  3. No follicles released
  4. Reduced oestrogen and
    progesterone levels in plasma (only
    small amounts of oestrogen and
    progesterone are synthesised in
    other organs)
  5. No development of the endometrial
    lining and no menstruation
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13
Q

“Hot flushes” are indicitive of menopause because:

A

No oestrogen-mediated inhibition of

GnRH & FSH release

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14
Q

Menopause pathway:

A
  1. Fail to recruit follicles by FSH
  2. Reduced estrogen, little progesterone & inhibin
  3. Negative feedback on hypothalamus and pituitary
  4. Increased GnRH (causes hot flushes) and
  5. Increased FSH and LH (due to lack of overriding negative feedback)
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15
Q

Oesterogen receptors:

A

ER(alpha) and ER(beta)

Located in the brain, bones, fat,
cardiovascular system, immune cells

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16
Q

Low endogenous levels of oestrogen

and progesterone lead to

A
  • Headaches
  • Mood disturbances
  • Depression
  • Fragile bones
  • Risk of cardiovascular disease
  • Change in immune function
  • Vaginal dryness
  • Thinning/dull hair
  • Weight gain
  • Bone pain (eg. Sore back)
  • Loss of muscle tone
  • Loose teeth
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17
Q

HRT patches are often used for women with:

A

A risk of blood clotting

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18
Q

Two different types of the contraceptive pill:

A
  1. The combined oestrogen and progestin pill

2. The progestin only pill

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19
Q

RULES OF THUMB:

Oral contraceptive

A

• Oestrogens should not be given without progestins to
women with a uterus

• In the absence of progestins, oestrogens cause
hyperproliferation of the endometrium of the uterus which
increases the risk of endometrial cancer

• Not a problem in post-hysterectomy women

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20
Q

Oestrogen component (combined pill)

A

• Natural oestrogen is more potent than
modified oestrogens, but is not well absorbed
from the gut and is rapidly cleared

• Original combined pill used high oestrogen
dose (150-50 ug), but this was associated with
a high incidence of side effects.

21
Q

Magic number for oestrogen dose:

A

20 ug
(effective and few side effects).

<20 ug = insufficient contraceptive effect

22
Q

Oestradiol

‘natural’ oestrogen

A

• Short half life (30 m)
• Metabolised in liver
and GI tract
• Less orally active

23
Q

Ethinylestradiol (EE)

A
  • Long half life (6-20h)

* More orally active

24
Q

HRT:

A

Conjugated Oestrogen:

Oestrone sulfate
• Metabolised in liver to
oestradiol via hydrolysis

Oestradiol
(‘natural’ oestrogen)
• Short half life (30 m)
• Metabolised in liver
and GI tract
• Less orally active
25
Q

Progestin component (combined or progestin only pill)

A

Progesterone
Norethiserone
Levorgestrel
Cypoterone acetate

26
Q

Progesterone:

A
  • Short half life (5 m)

* 100-200 mg

27
Q

Norethisterone:

A 
• Long half life (5-14h)
• Other family members
with slightly modified
structures
• 0.35 mg
28
Q

Levonorgestrel:

A
  • Long half life (~24h)

* 0.03/0.15 mg

29
Q

Cyproterone acetate:

A 
• Long half life (2-3 d)
• Potent anti-androgen
with progestin activity
• Also drospirenone
• 2 mg
30
Q

High plasma
estrogen

Very fluid.
Enhances sperm penetration

A

• Inhibits secretion of FSH (and
to a lesser extent, LH) via -ve
feedback (hypo & pit)

• Inhibits follicle maturation &
ovulation

31
Q

High plasma
progestin

Thick
Prevents sperm penetration

A

• Inhibits synthesis of LH at the
hypothalamus (-ve feedback)

• Prevents LH surge required for
ovulation, also…

• Thickens cervical mucus

• Forms a mucus ‘plug’ around
the cervix

• Prevents sperm from gaining
access to the uterus

32
Q

Hormone replacement for menopause: Estrogen

A

• Artificially add estrogen
(increase plasma levels)

• Negative feedback on
hypothalamus and pituitary

• Reduces GnRH, FSH and LH
(stops hot flushes)

• Replaces lost estrogen so maintains normal functioning
of all other cells that have
estrogen receptors

33
Q

Hormone replacement for menopause: Progestin

A
  • Artificially add progesterone (increased plasma levels)
  • Mimics luteal phase
  • Negative feedback on hypothalamus
  • Reduces GnRH secretion (stops hot flushes)

• No effect on plasma estrogen levels or cells containing
estrogen receptors. Generally positive effect on cells
containing progesterone receptors.

34
Q

Do not take oestrogen if you have a history of:

A
  • Hypertension
  • Stoke
  • Thromboembolism (DVT)
35
Q

Do not take progestin if you have:

A
  • Irregular vaginal bleeding

- ‘potentially’ higher contraceptive failure rate

36
Q

The emergency contraceptive induces:

A

Very high progestin

37
Q

The Emergency Contraceptive Pill: Levonorgestrel

A

c

Must be taken within 3-5 days (85% reduction in
conception within 3 days)

Works by:
- Preventing LH surge
- Prevents/delays ovulation
- Only works if taken 2 days before the LH surge
- Does NOT alter the capacity for ovum fertilisation or
implantation and DOES NOT effect the fetus.

Major side effects are menstrual irregularities, nausea &
vomiting (if vomiting occurs within several hours, another
pill is needed

38
Q

The Emergency Contraceptive: Levonorgestrel

A

Levonorgestrel 1.5 mg (compared to 0.15 mg)

Prevents LH surge
- Prevents/delays ovulation
- Only works if taken 2 days before the LH surge
- Does NOT alter the capacity for ovum fertilisation or
implantation and DOES NOT effect the fetus.

39
Q

The Emergency Contraceptive: Ulipristal 30 mg

A

Must be taken within 3-5 days (85% reduction in conception within 3 days)

Works by:
- Inhibiting progesterone binding to its receptor (exact
mechanism unknown)

  • Prevents or delays ovulation
  • Effect on implanted fertilised egg is unknown.

Major side effect is menstrual irregularities. Nausea &
vomiting are less common than for levonorgestrel)

40
Q

Deliberately inhibiting

hormone production treats:

A
  1. Pregnancy termination
  2. Treatment of Oestrogen receptor (ER) positive or ‘overexpressing’
    breast cancers
41
Q

~75% of breast cancers
overexpress ER –> promotes
tissue growth

A

~75% of breast cancers
overexpress ER –> promotes
tissue growth

42
Q

Pregnancy termination: Antiprogestin: Mifepristone

A
  • Competitive inhibitor of the progesterone receptor
  • Two fold higher affinity for the progesterone receptor than progesterone itself
  • Used as the first of a 2 step series of pills designed to medically terminate pregnancies
43
Q

Pregnancy termination: Antiprogestin: Mifeupristone 200mg

A

Causes breakdown of the decidua (what used to be the uterine endometrium)

Take a prostaglandin pill (which causes uterine contractions)

44
Q

Hormone therapy for

ER+ breast cancers:

A

Block oestrogen synthesis, or

Block oestrogen binding to the oestrogen receptors

45
Q

Oestrogens are produced by:

A
  1. Cholesterol is converted to progesterones (influence of LH)
  2. Progesterones are converted to androgens (LH)
  3. Androgens are converted to oestrogens (via aromatase UNDER influence of oestrogen)
46
Q

Aromatase inhibitors: Letrozole and Anastrozole

A

Competitively block
androgen binding to
aromatase active site

47
Q

How do oestrogens work?

A
  1. Oestrogen enters the cell by passive diffusion
  2. Binds to the oestrogen receptor (ER)
  3. Conformational change in the receptor
  4. Dimerizes with another oestrogen-bound ER
  5. Enters the nucleus
  6. Binds to the oestrogen responsive element (ERE)
    on DNA
  7. Conformational change allows binding of
    coactivators
  8. Binding of coactivators promotes gene
    transcription
48
Q

Oestrogen Receptor Inhibition: Tamoxifen

A
  1. Tamoxifen is metabolised to several ‘active’ forms
    (eg. 4-hydroxy tamoxifen) by liver CYP2D6 & 3A4
  2. 4-OH-Tam enters the cell
  3. Competitively binds to the oestrogen receptor
    (ER)
  4. NO conformational change in the receptor
  5. Dimerizes with another 4-OH-Tam bound ER
  6. Enters the nucleus
  7. Binds to the oestrogen responsive element (ERE)
    on DNA
  8. Lack of conformational change prevents binding
    of coactivators
  9. No gene transcription
49
Q

Tamoxifen

A

Acts as an ER antagonist in breast tissue (to slow breast cancer
growth) but acts as a partial agonist in the endometrium & bone

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