Endocrinology Part 4 - Gonadal Hormones Flashcards

1
Q

ovarian hormone synthesis

A

Ovarian Steroidogenesis

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2
Q

testicular hormone synthesis

A

Testicular Steroidogenesis

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3
Q

enzyme that converts cholesterol to pregnenolone

A

cholesterol side-chain cleavage enzyme

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4
Q

enzyme that converts pregnenolone to progesterone

A

3-beta-hydroxysteroid dehydrogenase

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5
Q

enzyme that converts progesterone to 17-OH progesterone

A

17-a-hydroxylase

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6
Q

enzyme that converts pregnenolone to 17-OH-pregnenolone

A

17-a-hydroxylase

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7
Q

enzyme that converts 17-OH-pregnenolone to 17-OH-progesterone

A

3-beta-hydroxysteroid dehydrogenase

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8
Q

enzyme that converts DHEA to androstenedione

A

3-beta-hydroxysteroid dehydrogenase

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9
Q

enzyme that converts 17-OH-pregnenolone to DHEA

A

17,20-Lyase

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10
Q

enzyme that converts 17-OH-progesterone to androstenedione

A

17,20-Lyase

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11
Q

enzyme that converts DHEA-S to DHEA

A

sulfotransferase

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12
Q

enzyme that converts androstenedione to testosterone

A

17-beta-hydroxysteroid dehydrogenase

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13
Q

enzyme that converts testosterone to dihydrotestosterone

A

5-a-reductase

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14
Q

where does conversion of testosterone → estradiol and androstenedione → estrone takes place?

A

Ovaries
Peripheral tissues (aside from testes & ovaries)

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15
Q

females have testosterone due to this presence

A

DHEA

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16
Q

events that occur in peripheral tissues during ovarian/testicular steroidogenesis

A
  • testosterone → (reduced) → dihydrotestosterone
  • adrenal androgen (DHEA) → testosterone
  • estriol (type of estrogen) → (hydroxylated) →estradiol
  • testosterone → estradiol
  • androstenedione → estrone
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17
Q

More potent than testosterone

A

Dihydrotestosterone

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18
Q

Responsible for masculinization of external genitalia (male gonads)

A

Dihydrotestosterone

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19
Q

What occurs when ↑ dihydrotestosterone in female

A

masculinization of female external genitalia

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20
Q

percentage of protein bound sex hormones

A

98-99%

cannot fuse to the vascular system → cannot interact with the target cells

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21
Q

percentage of free/unbound sex hormones

A

1-2%

biologically active

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22
Q

TRANSPORT PROTEINS OF GONADAL HORMONES

A

Sex Hormone-Binding Globulin (SHBG)
Corticosteroid-Binding Globulin (CBG)
Albumin

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23
Q

Transports androgens and estrogens

A

Sex Hormone-Binding Globulin (SHBG)

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24
Q

Binds adrenal cortex hormones

A

Corticosteroid-Binding Globulin

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25
Q

Delivers progesterone & glucocorticoids (cortisol)

A

Corticosteroid-Binding Globulin

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26
Q

Principal androgen hormone in the blood

A

TESTOSTERONE

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27
Q

Most potent androgen among male

A

TESTOSTERONE

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28
Q

T/F

testosterone is only found in men

A

F
Testosterone → estrogen among female

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29
Q

95% of testosterone are synthesized by

A

Leydig cells of testis

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30
Q

5% of testosterone are synthesized by

A

Conversion of DHEA → testosterone

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31
Q

Controlled primarily by the 2 stimulating hormone produced by pituitary gland such as FSH and LH

A

TESTOSTERONE

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32
Q

2 stimulating hormone produced by pituitary gland that controls testosterone production

A

FSH
LH

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33
Q

stimulating hormone that acts on the germinal stem cells of male

A

FSH (Follicle-stimulating hormone)

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34
Q

stimulating hormone that acts on the Leydig cells of male (stimulate cholesterol conversion to testosterone)

A

LH (luteinizing hormone)

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35
Q

T/F

Amount of testosterone is affected by some physiologic factors

A

T
Circadian rhythm, Obesity, Age

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36
Q

physiologic factors that affects testosterone amount

A

Circadian rhythm
Obesity
Age

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37
Q

Peak of testosterone levels are seen during

A

8 am (after waking up)

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38
Q

Lowest testosterone levels are seen during

A

8 pm

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39
Q

plasma testosterone of obese individuals

A

decreased

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40
Q

how does age affect testosterone production

A

gradual testosterone ↓ after 30 y/o = 110 ng/dL/decade ↓

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41
Q

For growth & development of male reproductive system

A

testosterone

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42
Q

Reference value of testosterone

A

3.9–7.9 ng/mL (serum)

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43
Q

Transport Protein of testosterone (w/ %)

A

Albumin (50%)
Sex Hormone-Binding Globulin (45%)

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44
Q

T/F
Transport protein measurement in male is essential
because binding proteins conc. can determine
testosterone level

A

T
↑ SHBG = ↑ testosterone

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45
Q

T/F

Free testosterone level can be measured in lab

A

F

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46
Q

Conditions under Hypergonadotropic Hypogonadism (Testosterone)

A

Klinefelter’s Syndrome (XXY)
5-reductase Deficiency
Myotonic Dystrophy
Sertoli cell-only deficiency/germ cell aplasia
Testicular Injury and Infection (mumps orchitis)
Testicular Feminization Syndrome

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47
Q

What type of hypogonadism is Hypergonadotropic Hypogonadism (Testosterone)

A

Primary hypogonadism

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48
Q

Hormone levels in Hypergonadotropic Hypogonadism (testosterone)

A

Low testosterone (stimulates FSH/LH production)
Elevated FSH/LH

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49
Q

Condition with Impaired sperm production → infertility/sterility

A

Hypergonadotropic Hypogonadism (testosterone)

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50
Q

Male individual with 3 sex chromosomes

A

Klinefelter’s Syndrome (XXY)

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51
Q

Presence of XX (female chromosomes) in males

A

Klinefelter’s Syndrome (XXY)

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52
Q

Normal 23rd pair of chromosomes in male

A

XY

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53
Q

Manifestations of Klinefelter’s Syndrome (XXY) due to presence of female chromosome (XX)

A

small firm testicles
gynecomastia (enlarged breast)
azoospermia (presence of semen with no sperm cell)

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54
Q

Condition with ↓ dihydrotestosterone

A

5-reductase Deficiency

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55
Q

Manifestation of 5-reductase Deficiency

A

Physical development similar to female phenotype
Cryptorchidism (presence of ambiguous/ undetermined genitalia)

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56
Q

Cryptorchidism is seen in what condition

A

5-reductase Deficiency

a Hypergonadotropic Hypogonadism (testosterone)

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57
Q

Characterized by muscle dystonia and testicular failure (esp. at 4th decade of life)

A

Myotonic Dystrophy

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58
Q

involuntary muscle contraction

A

Muscle dystonia

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59
Q

Testicular failure in myotonic dystrophy usually occurs during this period of life

A

4th decade of life

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60
Q

aka Sertoli cell-only deficiency

A

germ cell aplasia

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61
Q

reason of lacking germ cell in Sertoli cell-only deficiency

A

Aplasia – no cell growth → lack of germ cell

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62
Q

Biopsy of small testis of this condition presents an absence of spermatozoa

A

Sertoli cell-only deficiency/germ cell aplasia

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63
Q

Manifestations and hormone levels in Sertoli cell-only deficiency/germ cell aplasia

A

small testis
azoospermia

↑ FSH
N/↓ - testosterone

64
Q

Example of Testicular Injury and Infection

A

Mumps orchitis

65
Q

scrotum inflammation due to mumps infection

A

Mumps orchitis

66
Q

mechanism of how mumps can cause testicular injury or infection

A

parotitis/mumps (beke) in males → mumps migrates to scrotum, causing inf. → infertility

67
Q

Most severe form of androgen resistance

A

Testicular Feminization Syndrome

68
Q

testosterone level in Testicular Feminization Syndrome

A

Normal

69
Q

Target tissue does not react in response to testosterone (resistance) – NO RECEPTORS

A

Testicular Feminization Syndrome

70
Q

Manifestation of Testicular Feminization Syndrome

A

Female-like genitalia w/ intraabdominal testis

71
Q

Hormone levels in Hypogonadotropic Hypogonadism (Testosterone)

A

Low testosterone
Low/N FSH or LH

72
Q

Conditions under Hypogonadotropic Hypogonadism (testosterone)

A

Kallman’s Syndrome
Hyperprolactinemia
Type 2 Diabetes
30 y/o age
Opioid use
Pituitary Disease
Obstructive Sleep Apnea

73
Q

Manifestation of hypogonadism at puberty

A

Kallman’s Syndrome

74
Q

has a manifestation of Red-green color blindness

A

Kallman’s Syndrome

75
Q

has a manifestation of anosmia (a cerebral dysfunction)

A

Kallman’s Syndrome

76
Q

Manifestations of Kallman’s Syndrome

A

Cleft palate/lip
Red-green color blindness
Deafness
Cerebral dysfunction: anosmia (inability to smell; impaired olfactory sensors)

77
Q

GnRH inhibitor that leads to Hypogonadotropic Hypogonadism (testosterone)

A

PRL
Opioid (narcotics)

78
Q

mechanism why hyperprolactinemia causes Hypogonadotropic Hypogonadism (testosterone)

A

↑ PRL inhibits FSH/LH production →hypogonadism

PRL – GnRH inhibitor

79
Q

Principal adrenal androgen

A

Dehydroepiandrosterone (DHEA)

80
Q

Weak adrenal androgen must be converted to a more
potent androgen –> DHEAS

A

Dehydroepiandrosterone (DHEA)

81
Q

Used as valuable assessment for adrenal cortex function

A

Dehydroepiandrosterone (DHEA)

82
Q

Most potent female hormone

A

ESTROGEN

83
Q

Arises through structural alteration of testosterone molecule

A

ESTROGEN

84
Q

Promote breast, uterine, and vaginal development

A

ESTROGEN

85
Q

Types of Estrogen

A

Estrone (E1)
Estradiol (E2)
Estriol (E3)

86
Q

Most abundant estrogen form in post-menopausal women

A

Estrone (E1)

87
Q

Most potent estrogen

A

Estradiol (E2)

88
Q

Principal estrogen form

A

Estradiol (E2)

89
Q

Used to assess ovarian function

A

Estradiol (E2)

90
Q

Estradiol level in menopausal women?
Estradiol level in pre-menopausal women?

A

↓: menopausal women

↑: pre-menopausal women

91
Q

Estrogen form found in maternal urine

A

Estriol (E3)

92
Q

Fetoplacental viability marker

A

Estriol (E3)

93
Q

Down Syndrome marker (others: AFP, hCG)

A

Estriol (E3)

94
Q

metabolites of intraovarian testosterone conversion

A

E1 & E3

95
Q

Progesterone is ONLY produced by

A

corpus luteum

96
Q

Prime secretory product of the ovary

A

PROGESTERONE

97
Q

Dominant hormone responsible for the luteal phase

A

PROGESTERONE

98
Q

Prepares the endometrium for embryo implantation

A

PROGESTERONE

99
Q

Single best hormone to determine whether ovulation has occurred

A

PROGESTERONE

100
Q

What happens when progesterone is deficient

A

failure to embryo implantation (miscarriage)

101
Q

cycle of shedding of uterine lining from the previous cycle among non-pregnant women (no point of start and point of end)

A

Menstruation

102
Q

2 phases of menstruation

A

Follicular phase
Luteal phase

103
Q

Starts at the onset of menstruation (1st day of menstruation occur when luteal phase ends)

A

Follicular phase

104
Q

Menstrual phase that lasts for 14 days

A

Follicular phase

105
Q

Involves ↑ FSH = ↑ estrogen (positive feedback system) = ↑ LH (LH surge)

A

Follicular phase

106
Q

Event that occur in the 14th day of follicular phase

A

LH surge

107
Q

Starts 36 hrs after LH surge

A

Luteal phase

108
Q

↑ LH will stimulate ovulation in this phase

A

Luteal phase

109
Q

↑ LH will stimulate ovulation (release of ovum from the ovary) in luteal phase causes?

A

luteinization of corpus luteum

110
Q

what happen when there is NO fertilization

A

Shedding of thickened endometrium – NO embryo is implanted

111
Q

what happen when there is fertilization

A

↑ hCG secreted by placenta

pregnancy test sample: urine

112
Q

Shedding of endometrium is due to this hormone

A

↑ progesterone

113
Q

Occur 14 days after ovulation at 28th day

A

Shedding

114
Q

Lasts for 3-5 days

A

Shedding

115
Q

first day of mens (start of follicular phase; end of luteal phase)

A

Shedding

116
Q

T/F

Shedding occur for 3-5 days but does not mean that it is the end of follicular phase (lasts for 14 days)

A

T

117
Q

T/F

Few days after menstruation, female is fertile

A

T

LH surge presence → ovulation presence

118
Q

Menstrual Cycle Abnormalities

A

Amenorrhea
Oligomenorrhea
Menorrhagia

119
Q

Absence of menstruation

A

Amenorrhea

120
Q

Primary Amenorrhea occurs during this age

A

16 y/o

121
Q

occurs when women had 1 menstrual cycle followed by absences of menstruation for 3-6 mos

A

Secondary Amenorrhea

122
Q

Infrequent irregular menstrual bleeding

A

Oligomenorrhea

123
Q

Interval betw 2 mens in Oligomenorrhea?
what is the normal interval?

A

35-40 days

Normal: 28 days

124
Q

Menstruation that occurs for >7 days

A

Menorrhagia

125
Q

Excessive shedding

A

Menorrhagia

126
Q

What is the defect when there is Hypergonadotropic Hypogonadism (female hormones)

A

ovaries (primary hypogonadism)

127
Q

hormone levels in Hypergonadotropic Hypogonadism (female hormones)

A

Low female hormone
↑ FSH
Normal/↑ LH

128
Q

Conditions under Hypergonadotropic Hypogonadism (female hormones)

A

Menopause
Premature ovarian failure
Turner’s syndrome (X ) or (X, partial X)

129
Q

physiologic event among female where menstrual cycle stops

A

Menopause

130
Q

Menopause occurs at this age range

A

45-55 y/o (American women)

131
Q

Genetic defect (one X or X with partial X chromosome)

A

Turner’s syndrome

132
Q

Hypogonadotropic Hypogonadism (female hormones) is aka? reason?

A

Gonadotropin deficiency

FSH and LH are gonadotropins

133
Q

category of Hypogonadotropic Hypogonadism (female hormones)

A

Secondary hypogonadism

134
Q

Low female hormone due to low gonadotropins

A

Hypogonadotropic Hypogonadism/Gonadotropin deficiency

135
Q

Conditions under Hypogonadotropic Hypogonadism/Gonadotropin deficiency

A

Anorexia nervosa
Runner’s amenorrhea
Prolactinoma
Athlete’s triad

136
Q

Hypogonadotropic hypogonadism that results to weight loss

A

Anorexia nervosa

*female hormones

137
Q

Associated with females who undergo intense physical exercise → leads to absence of menses

A

Runner’s amenorrhea

*Hypogonadotropic hypogonadism (female hormones)

138
Q

mechanism of how prolactinoma causes Hypogonadotropic hypogonadism (female hormones)

A

GnRH inhibitor → ↓ FSH and LH

139
Q

Included in Athlete’s triad

A

Amenorrhea
Eating disorder
Osteoporosis

140
Q

aka Polycystic Ovarian Syndrome (PCOS)

A

Enlarged ovaries

141
Q

Former name of PCOS

A

Stein-Leventhal Syndrome

142
Q

Common among female characterized by multiple ovarian cysts (70% of patients)

A

Polycystic Ovarian Syndrome (PCOS)/Enlarged ovaries

143
Q

T/F

NOT all have ovarian cysts (30% of patients) in PCOS

A

T

144
Q

Associated with infertility and other menstrual irregularities

A

Polycystic Ovarian Syndrome (PCOS)/Enlarged ovaries

145
Q

T/F

PCOS individuals are often overweight

A

T

146
Q

T/F

PCOS is irreversible

A

F

Reversed with weight loss, increased physical activity, Metformin

147
Q

Polycystic Ovarian Syndrome (PCOS)/Enlarged ovaries is reversed with?

A

Weight loss
Increased physical activity
Metformin

148
Q

antidiabetic drug for PCOS? how does it affect PCOS?

A

Metformin

acts as insulin sensitizer (↑ cell sensitivity to insulin) since PCOS individuals have insulin resistance

149
Q

Mechanism why PCOS often leads to virilization and inhibits ovulation

A

PCOS individuals have insulin resistance (resembles Type 2 DM). Therefore, INCREASED insulin

↑ insulin = ↑ testosterone

High testosterone level leads to virilization (hirsutism) & inhibits ovulation

150
Q

Excess hair along the midline of the female body

A

Hirsutism

151
Q

Hirsutism is caused by increased levels of

A

androgens

152
Q

used to diagnose hirsutism by assessing 9 areas of the body

A

Ferriman-Gallwey Scale

153
Q

Ferriman-Gallwey Scale specifically assess

A

Hair thickness
Hair pigmentation

154
Q

9 areas of the body assessed by Ferriman-Gallwey Scale

A
  1. Lip
  2. Chin
  3. Side burns
  4. Neck
  5. Chest
  6. Abdomen
  7. Upper back
  8. Lower back
  9. Thighs
155
Q

Scoring of Ferriman-Gallwey Scale

A

0 - 4

156
Q

scoring if there is hirsutism using Ferriman-Gallwey Scale

A

> 8