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Clinical Embryologist's exam samples. > COH & Endocrinology > Flashcards

COH & Endocrinology Flashcards

1
Q

The Phase where the follicle develops is called

A

Follicular Phase

Characterized By:

Low FSH

Low LH

Elevated Estrogen (E2)

Low Progesterone (P)

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2
Q

The Phase when follicle development is complete and the mature oocyte is shed is called

A

Ovulation

characterized by:

Elevated FSH

Elevated LH

Elevated Estrogen (E2)

Rising Progesterone (P)

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3
Q

The phase when the embryo attaches is called

A

The Luteal Phase

characterized by:

Low FSH

Low LH

Elevated Estrogen (E2)

Elevated Progesterone (P)

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4
Q

The Phase When the Uterine Tissue is Shed and Follicle Recruitment begins

A

Menses

Characterized by

Elevated FSH

Low LH

Low Estrogen (E2)

Low Progesterone (P)

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5
Q

The uterine lining in the follicular phase is said to be:

A

Proliferative

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6
Q

The Uterine Lining In The Luteal Phase is:

A

Secretory

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7
Q

GnRH is released from the hypothalamus;
low frequency pulses ►stimulate the pituitary to release→ FSH

and high frequency pulses ►to release ⇒LH.

A

true

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8
Q

During the follicular phase, GNRH is released about every:

A

60-90 minutes

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9
Q

After Ovulation, GnRH is released about every:

A

120 Min

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10
Q

The target for GnRH is:

  1. The Hypothalamus
  2. The Anterior Pituitary
  3. The Posterior Pituitary
  4. The Ovary
  5. The Uterus
A

2.

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11
Q

The primary aim of GNRH secretion is the release of:

  1. GnRH
  2. TSH
  3. FSH
  4. LH
  5. hCG
  6. Prolactin
  7. Oestradiol
  8. Progesterone
A

3 and 4

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12
Q

Which group of compounds can inhibit GnRH Secretion

  1. Clomiphene
  2. Letrozole
  3. GnRH Antagonists
  4. GnRH Agonists
  5. Kisspeptin
A

3, 4 and 5

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13
Q

Which group of compounds can inhibit GNRH activity by disrupting the frequency of secretion:

  1. Clomiphene
  2. Letrozole
  3. GnRH Antagonists
  4. GnRH Agonists
  5. Kisspeptin
A

4.

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14
Q

Which group of compounds can inhibit GNRH activity by binding to the receptor for GNRH:

A

GnRH Antagonist

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15
Q

The Hypothalamus receives stimulation from:

A

The central nervous system (CNS)

Amygdala, visual cortex and the olfactory cortex

Endrocrine factors from the testis, ovary and other endocrine glands

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16
Q

The trigger for ovulation, the LH surge is triggered by

A

rising estradiol

increasing frequency of GnRH secretion

Removal of GnRH Attenuation Factors

A mature follicle(s)

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17
Q

FSH normal value?

A

<8 IU/L

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18
Q

LH normal value

A

<10 IU/L

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19
Q

Estradiol: Early Follicular Is:

A

50-200 pmol/L

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20
Q

Estradiol (Mid-Cycle) normal value….

A

50-1000pmol/L

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21
Q

Progesterone (Mid-Luteal)

A

>40 nmol/L

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22
Q

Testosterone NV:

A

0.5-3.0 nmol/L

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23
Q

Sex Binding Globulin (SHBG)

A

16-119 nmol/L

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24
Q

Free Androgen Index (FAI) is:

A

< 5

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25
Q

TSH

A

0.5-5.5 nmol/L

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26
Q

Prolactin

A

< 600 mIU/L

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27
Q

AMH may be used to:

  1. predict the ovarian response to hyperstimulation
  2. the timing of menopause
  3. to indicate iatrogenic damage to the ovarian follicle reserve
  4. a surrogate for antral follicle count (AFC)
  5. diagnosis polycystic ovary syndrome (PCOS)
A

all correct

28
Q

AMH is Produced by

  1. Primoidial follicles
  2. Primary follicles
  3. Secondary PreAntral follicles
  4. Small antral follicles
  5. Large selected follicles
  6. Pre-ovulatory Graffian Follices
29
Q

A high AMH implies:

  1. PCOS
  2. A good response to ovarian stimulation
A

all correct

30
Q

A Low AMH implies

  1. PCOS
  2. A good response to ovarian stimulation
  3. A normal response to ovarian stimulation
  4. A poor response to ovarian stimulation
  5. Little or no response to ovarian stimulation
  6. Menopause
31
Q

AMH may be useful in:

A

assessing the need for fertility preservation strategies

detecting post-chemotherapy or surgical damage to the ovarian reserve

the time to menopause

32
Q

Which protocol starts GNRH agonist/antagonist on day 21 of the previous cycle

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
33
Q

Which protocol starts GNRH agonist/antagonist on day 2 of the previous cycle

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
34
Q

Which protocol starts GNRH agonist/antagonist on day 2 of the treatment cycle

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
35
Q

Which protocol starts GNRH agonist/antagonist on or after day 6 of the treatment cycle

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
36
Q

Which protocol continues GNRH agonist/antagonist until the HCG ovulation trigger

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
A

1, 2, 3, 5

37
Q

which protocol continues GNRH agonist/antagonist for 3 days

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
38
Q

Which protocol controls pituitary FSH secretion by disrupting the normal cyclic secretions of GNRH by the Hypothalamus

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
A

1, 2, 3 and 4

39
Q

Which protocol controls causes a surge or flare in pituitary FSH secretion before slowly fading to low levels

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
A

1, 2, 3 and 4

40
Q

Which protocol controls results in a long delay in resumption pituitary FSH/LH secretions

  1. Long GnRH agonist protocol
  2. Follicular phase GnRH agonist protocol
  3. Short GnRH agonist protocol
  4. Ultra Short GnRH agonist protocol
  5. GnRH antagonist protocol
A

1, 2, and 3

41
Q

Which protocol controls pituitary FSH secretion by competing with the pituitary receptor for GNRH

A

GnRH antagonist protocol

42
Q

Which protocol may NOT suppress ovulation

A

Ultra Short GnRH agonist protocol

43
Q

Which protocol significantly depletes LH secretions as well as FSH in a manner that may not support follicle development

A

GnRH antagonist protocol

44
Q

Clomiphene acts on

  1. FSH Receptors in the hypothalamus
  2. FSH Receptors in the pituitary
  3. FSH receptors in the uterus
A

all correct

Clomiphene was the first form of COH employed in IVF in early 1980’s

45
Q

Clomiphene’s main action is to

  1. Stop GnRH secretions
  2. Stop FSH secretions by the pituitary
  3. Stop the feedback suppression of FSH secretions caused by rising follicle derived oestradiol
  4. Desensitise the pituitary to rising follicle dereived oestradiol
  5. Trick the pituitary into thinking there are no growing follicles and continue to release FSH
46
Q

Clomiphene is usually given between

  1. Days 1-3 of the cycle
  2. Days 1-5 of the cycle
  3. Days 2-5 of the cycle
  4. Days 2-6 of the cycle
  5. Days 3-6 of the cycle
47
Q

Clomiphene May delay uterine development during administration

48
Q

Clomiphene may mask any Estrogen dependent actions during administration

49
Q

Clomiphene► When used in ART as a cheaper or mild stimulation tool, the HCG trigger may need to be given earlier to avoid precocious ovulation

A

true

Clomiphene in Ovulation induction►

There is a risk of multiple pregnancy when used in IUI or Ovulation Induction

50
Q

Clomiphene may be used in ART for patients who do not fully suppress with GnRH Agonists/Antagonists

51
Q

Which of the following are GnRH Agonists

  1. Clomiphene
  2. Decapeptyl
  3. Zoladex
  4. Buserelin
  5. Nafarelin
  6. Syneral
  7. Cetrorelix
  8. Ganirelix
A

2, 3, 4, 5. and 6

GnRH Agonists

  • Decapeptyl
  • Zoladex
  • Buserelin
  • Nafarelin
  • Syneral
52
Q

Which of the following are GnRH Antagonists

  1. Clomiphene
  2. Decapeptyl
  3. Zoladex
  4. Buserelin
  5. Nafarelin
  6. Syneral
  7. Cetrorelix
  8. Ganirelix
A

7 and 8

GnRH Antagonists

  • Cetrorelix
  • Ganirelix
53
Q

Which of the following are administered as a daily injection

  1. Clomiphene
  2. Decapeptyl
  3. Zoladex
  4. Buserelin
  5. Nafarelin
  6. Syneral
  7. Cetrorelix
  8. Ganirelix
A

4, 7 and 8

54
Q

Which of the following are administered as a depot injection

  1. Clomiphene
  2. Decapeptyl
  3. Zoladex
  4. Buserelin
  5. Nafarelin
  6. Syneral
  7. Cetrorelix
  8. Ganirelix
A

2 and 3

depot injection

a sustained-action drug formulation that allows slow release and gradual absorption

55
Q

Which of the following are administered as a daily intranasal sniff

  1. Clomiphene
  2. Decapeptyl
  3. Zoladex
  4. Buserelin
  5. Nafarelin
  6. Syneral
  7. Cetrorelix
  8. Ganirelix
A

3, 6 and 8

56
Q

Which of the following are TRUE

  1. Agonist cause a transient rise in FSH as the pituitary starts to desensitize to GnRH
  2. After this flare in FSH secretions, the pituitary secretions of FSH slowly decline over several days
  3. Long Agonist protocols cause the flare to occur before FSH treatment starts
  4. Some residual serum FSH and LH pituitary activity is always present during stimulation
  5. Sufficient pituitary LH is present after long down regulation to maintain follicle health
57
Q

Which of the following are TRUE

  1. Pituitary FSH secretion ceases shortly after antagonists are administered
  2. Antagonists are mainly used to suppress a LH Surge
  3. Pituitary FSH and LH secretions resume shortly after the antagonist is withdrawn
  4. A similar number of injections are needed in agonist and antagonist regimens
  5. The pregnancy rate is double using Antagonists protocols
  6. 95% of all IVF cycles use an antagonist regimen
  7. Starting the antagonist may cause a severe decline in LH secretion effecting E2 output
  8. Many think the antagonist is a more natural regimen
A

1,2, 3, 7 and 8

58
Q

Prior to starting FSH Stimulation, many protocols call for an ultrasound assessment to confirm there are no physical limitations. which of the following need to be checked?

A

The size and position of each ovary

The accessibility and suit of both ovaries for follicle aspiration

The presence of residual corpus luteum

Endometrial or other cycts

The location of the uterus and the appearance of the endometrium

Evidence of PCO

The presence of Fibroids

The presence of hydrosalpinges or uterine fluid

Congenital or other abnormalities

59
Q

Poor Responder:

  1. imply an intrinsic inability of a woman’s ovaries to react accordingly to the stimulation chosen
  2. imply an intrinsic inability of a woman’s ovaries to react regardless to the stimulation chosen
  3. implies that pregnancy will never happen
60
Q

which may be true:

  1. POR (poor ovarian response) may be an early sign of reduced ovarian reserve
  2. POR may be an early sign of ovarian ageing
  3. ovarian stimulation can be viewed as a dynamic test for the resting ovarian follicular pool.
  4. the size of the cohort of recruitable follicles may be a reflection of the resting follicle pool
61
Q

For a cycle or attempt to be considered to have been a poor response, what criteria need to be met?

A

Advanced maternal age (+40 years) or any other risk factor for POR

A previous POR (<4 oocytes with a conventional stimulation protocol)

An abnormal ovarian reserve test

  • AFC ,5–7 follicles
  • AMH 0.5 –1.1 ng/ml).
62
Q

For a woman to be considered a poor responder (PORs), she should had one stimulated cycle with maximal stimulation.

63
Q

** However, if a women was over 40 years of age and had an abnormal ovarian reserve test (AMH or AFC), then this may act as a surrogate stimulation cycle, for the purposes of defining a woman as a poor responder.**

64
Q

AMH Levels in women who are Carriers of the BRAC1 Mutation are:

A
  • 25% lower than non carriers
65
Q

Alpha-fetoprotein (AFP)
Abnormal AFP levels can be indicative of certain conditions during pregnancy:
a- AFP is an old screening method not widely available.
b- normal value of AFP ranges between 110-120 ng/mL
c- AFP can be measured for adults only to detect liver cancer markers
d-Increased or decreasd AFP levels in maternal blood can be indicative of certain conditions during pregnancy

A
  1. is correct
    Elevated AFP levels in maternal blood can be associated with conditions such as neural tube defects (NTDs) and abdominal wall defects in the fetus.
    On the other hand,
    low AFP levels may be associated with chromosomal abnormalities (DS)

Clinical Embryologist's exam samples. (22 decks)

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