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Pathophysiology > Reproductive Disorders > Flashcards

Reproductive Disorders Flashcards

1
Q

the corpus lute produces __________
the placenta produces ___________________

A

progesterone

estrogens and progesterone

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2
Q

5a reductase

A

catalyzes the formation of DHT from testosterone in the prostate gland, seminal vesicles, epididymides, skin, hair follicles, liver and brain

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3
Q

DHT is considerably

A

more potent agonist than testosterone for androgen reeptor

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4
Q

which hormones are responsible for the gonads?

A

GnRH –> FSH and LH –> gonads

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5
Q

testes do not synthesize

A

aldosterone and cortisol

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6
Q

enzyme that converts testosterone to estradiol

enzyme that converts androstenedione to estrone

A

aromatase (both)

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7
Q

enzyme that converts androstenedione to testosterone

A

17b - hydroxysteroid dehydrogenase

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8
Q

enzyme that converts testosterone to dihydrotestosterone

A

5a - reducatase

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9
Q

chromosomal sex

A

determination of an individual’s sex based on the combination of sex chromosomes in their cells

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10
Q

genetic sex is established at

A

fertilization by the kind of sperm that fertilizes the ovum

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11
Q

when do the gonads begin to attain sex characteristics?

A

7th week

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12
Q

indifferent state of sexual development

A

early genital systems in two sexes are similar

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13
Q

Y chromosome

A

SRY (sex determining region Y)
gene codes for the testis determining factor

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14
Q

in the absence of SRY there are

A

no testes

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15
Q

X chromosome

A

DSS (dosage sensitive sex reversal)
double dose gene

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16
Q

how many DSS genes are required for the ovaries to be fully functional?

A

2

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17
Q

SRY

A

transcription factor
master gene for testes development

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18
Q

SRY possibly acts in conjugation with ____________ which induces ________________

A

SOX9

testes differentiation

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19
Q

SRY and SOX9 induce the testes to secrete _____________ that causes the tubules from the mesonephric duct to ________________

A

fibroblast growth factor 9

penetrate the gonadal ridge

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20
Q

without penetration of the gonadal ridge by the tubules,

A

differentiation of the testes does not continue

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21
Q

SRY directly or indirectly through SOX9 up regulates production of

A

stetoidogenesis factor 1

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22
Q

stetoidgenesis factor 1 (SF1) stimulates

A

differentiation of stertoli and Leydig cells

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23
Q

SF1 and SOX9 increase anti-Mullerian hormone leading to

A

regression of the paramesonephric ducts

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24
Q

SF1 upregulates

A

the genes for enzymes that synthesize testosterone

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25
Q

gonadal development occurs ___________ in females

A

slowly

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26
Q

what forms into the ovarian medulla

A

irregular cell clusters are replaced by a vascular storm –> formation

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27
Q

surface epithelium of the female gonad, unlike males, ________________ giving rise to a ________________________ in the 7th week

A

continues to proliferate

second generation of cords (cortical cords)

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28
Q

cortical cords

A

penetrate the underlying mesenchyme but remain close to the surface

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29
Q

descendants of the surface epithelium form

A

follicular cells

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30
Q

germ cells (females) develop into

A

oogonia

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31
Q

when do cortical cords split into isolated cell clusters

A

4th month

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32
Q

sex differentiation depends upon the formation of two important hormones

A

secretion of AMH
secretion of androgens

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33
Q

what degenerates when there is secretion of AMH?

what degenerates when there is absence of testosterone?

A

mullerian duct

wolffian duct

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34
Q

if testes are developing normally,

A

Sertoli cells produce AMH

leading cells start secreting androgens

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35
Q

if ovaries are developing normally,

A

no production of androgens (loss of wolfarian ducts)

ovaries do not produce AMH, develop Mullerian ducts

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36
Q

three categories of sex organs

A

gonads
internal sex organs
external sex organs

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37
Q

gonads (testes or ovaries)

A

develop first
produce ova/sperm and secret hormones

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38
Q

when is the critical period of sexual development for the gonads?

A

gestational weeks 7-12

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39
Q

gonads develop as a function

A

of the presence or absence of SRY gene

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40
Q

when do the testes develop? what part degenerates?

for the ovaries?

A

7th week, outer portion

11th week, inner portion

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41
Q

mullerian system

A

females
composed of mullein ducts that later become the uterus, fallopian tubes and the upper part of the vagina

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42
Q

wolffian system

A

males
composed of wolffian ducts that later become epididymis, vas deferens, seminal vesicles

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43
Q

androgen insensitivity syndrome

A

genetic mutation that prevents the formation of androgen receptors
abnormal process - lack of masculinization

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44
Q

what would an XY male with androgen sensitivity syndrome look like?

A

female external genitalia
has a woman’s body but not internal female sex organs

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45
Q

persistent mullerian duct syndrome

A

failure to produce anti-mullerian hormone
absence of receptors for this hormone

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46
Q

what would an XY male with persistent Müllerian duct syndrome look like?

A

defeminization does not occur but masculinization does
both sets of internal sex organs

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47
Q

turner’s syndrome

A

individuals only have one sex hormone (X)
develop into females but no ovaries since XX needed

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48
Q

Pubery

A

development of secondary sex characteristics

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49
Q

when does puberty occur

A

when the hypothalamus begins to secrete gonadotropin releasing hormone (GnRH)

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50
Q

what does GnRH release

A

follicle stimulating hormone (FSH)
Luteinizing hormone (LH)

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51
Q

what affects the age of puberty?

A

nutrition
(thinner - presence of leptin –> puberty later)

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52
Q

main function of the male reproductive system

A

produce and deliver sperm to the female reproductive system

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53
Q

how many sperm does a healthy male typically produce?

A

1500/s

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54
Q

testes

A

make sperm and testosterone
produce 100+ million sperm/day after puberty
sperm develop best few degrees below 98.6

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55
Q

seminiferous tubules

A

tightly coiled tubes inside the testes where sperm are made
contain Sertoli cells to convert spermatocytes to spermatozoa

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56
Q

SRY initiates differentiation of ______________________ and these produce _________________ which causes _______________

A

epithelial cells to Sertoli cells

anti mullerian hormone

deterioration of the Müllerian duct (defeminization)

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57
Q

Mesenchyme cells differentiate into _____________ which produce _______________ responsible for the development and differentiation of the _________________

A

leydig cells

androgens

wolffian duct

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58
Q

5-dihydrotestosterone

A

responsible for masculine development of external genitalia

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59
Q

in response to LH, ______________ produce testosterone

A

Leydig cells

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60
Q

in response to FSH and testosterone, _________________ support spermatogenesis

A

Sertoli cells

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61
Q

prostate gland

A

accessory sex organ that contains 5a reductase

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62
Q

inhibitors of 5a reductase

A

finasteride
therapy for benign prostatic hypertrophy

63
Q

why do the testes descend into the scrotum after birth?

A

because sperm need a cooler temperature to develop

64
Q

sperm are delivered into the ________________ where they must remain for at least ____________ for mobility to develop, then pass into the __________________

A

epididymis

18 hours

vas deferens

65
Q

seminal vesicles produces ________________
prostate gland produces _________________

A

fructose-rich fluid

milky fluid (semen)

66
Q

because boys begin their final growth spurt later than girls,

A

they have a longer period of steady growth

usually attain a greater adult height

67
Q

what are testosterone plasma levels before puberty?

A

very low

68
Q

after puberty, there is progressive more frequent and greater amplitude of

A

GnRH release

69
Q

Azoospermia

A

no sperm count in ejaculate
2% of the general male population
loss of small proportions of AZF region

70
Q

obstructive azoospermia (post testicular azoospermia)

A

no sperm are seen in the semen due to ejaculatory duct obstruction, which allows exit to the exterior

71
Q

Testicular feminization (Androgen Insensitivity syndrome/Morris syndrome)

A

affects the development of a child’s genitals and reproductive organs
born XY but abnormalities lead to resistance to actions of androgen hormones

72
Q

Kallmann Syndrome (KS)

A

Delayed or absent puberty and impaired sense of smell

73
Q

KS at puberty

A

Do not develop secondary sex characteristics
No facial hair, deep voice, periods, breasts, growth spurts

74
Q

a child born with ASI is generally ___________, but the external appearance of their genitals may be

A

male

female or somewhere between male and female

75
Q

ASI can be

A

complete (appears to be a woman) or
incomplete (various sexual ambiguities)

76
Q

Can someone with KS have children?

A

Not without treatment

77
Q

characteristics of ASI

A

normal breast development
narrow hips
little armpit/pubic hair
absence of uterus
testicular atrophy
short vagina with blind termination

78
Q

Klinefelter’s syndrome

A

can be dominant or recessive (XXY)
1 in 400 males
caused by nondisjunction
often under diagnosed

79
Q

What causes KS?

A

Failure of hypothalamus to release GnRH at appropriate time, GnRH releasing neurons do not migrate to correct location
Mutation in X-linked KAL1 gene

80
Q

can Klinefelter’s syndrome be treated?

A

yes with male hormones

81
Q

Klinefelter’s syndrome characteristics

A

lower IQ than sibs
tall stature
poor muscle tone
reduced secondary sex characteristics
gynaecomastia
small testes/infertility

82
Q

because there is low _______ in Klinefelter’s syndrome, this may lead to

A

IQ

language difficulties, slow motor development, learning and language problems

83
Q

Treatment for males with KS

A

Repeated GnRH injections promote spermatogenesis
Combine hCG injections with FSH

84
Q

Mutations in SRD5A2 gene

A

Cause 5-alpha reductase deficiency

gene responsible for making the enzyme

85
Q

Testosterone gets converted into ____ by ____ then binds to ____ receptor and triggers ____ ____.

A

DHT

5-alpha reductase

androgen

hair loss

86
Q

5-alpha reductase leads to normal growth and function of the

A

the prostate are contingent on this to reduce testosterone to DHT

87
Q

Overabundance of DHT

A

Benign prostatic hyperplasia (BPH)
Prostate cancer

88
Q

Inhibition of 5-AR

A

Useful in treatment of BPH in reducing risk of prostate cancer

89
Q

congenital anomalies of the penis

A

hypospadias
agenesis of external geniralia
bifid penis and double penis
micropenis

90
Q

congenital anomalies of the testes

A

undescended testes (cryptochidism)
hydrocele
scrotal anomalies

91
Q

the basic etiology of ASI is a

A

loss of function mutation in the androgen receptor gene localized on the X chromosome

92
Q

gene responsible for short stature in Klinefelter syndrome

A

SHOX (short stature homeobox containing gene)

93
Q

in kallmann syndrome, why is there failure of the hypothalamus to release GnRH?

A

the cells responsible for production of GnRH did not migrate from the olfactory epithelium to the pituitary gland

94
Q

treatment of females with KS

A

hormone therapy to stimulate the ovaries mildly

95
Q

5 a reductase inhibitors can be used to treat

A

hair loss

96
Q

when there is absence of AMH, there is development of ________________ which leads to the formation of

A

Müllerian ducts

uterus, fallopian tubes, and upper vagina

97
Q

Organ most affected during GDM

A

Placenta
Need glucose to feed placenta

98
Q

estradiol leads to the formation of

A

clitoris
labia minora and majora
lower vagina

99
Q

estradiol secondary sex characteristics

A

increased size of female sex organs
enlarged breasts
skeleton changes
increased protein deposition and metabolic rate
increased fat deposition
hair distribution
thickening of skin
electrolyte balance

100
Q

Glucose in normal pregnancy

A

Slow down of insulin sensitivity
Slight increase in glucose
Normal levels after birth

101
Q

Glucose in GDM pregnancy

A

Extreme slow down of insulin
Extreme increase in glucose
May remain high after birth

102
Q

progesterone secondary sex characteristics

A

inc glandular function of uterus
inc glandular secretions of fallopian tubes
swelling of breasts

103
Q

Miscarriage

A

Spontaneous abortion before 24 weeks gestation

104
Q

theca cells

A

produce androgens that diffuse into the granulosa cells

105
Q

Ectopic pregnancy

A

Implantation of blastocytes into lining of fallopian tube instead of endometrium
Embryo not viable

106
Q

FSH acts on granulosa cells to stimulate

A

aromatase activity, which converts androgens to estrogens

107
Q

why can’t granulosa cells produce androgens?

A

they lack the enzyme that converts progesterone to androgens

108
Q

Vaginal bleeding in third trimester

A

Placenta previa
Placenta abruption

109
Q

similarities between theca cells and granulosa cells

A

LH receptors

110
Q

theca cells lack aromatase which means they cannot synthesize

A

estrogens

111
Q

Trophoblastic Diseases (GTD)

A

Molar pregnancy most common

112
Q

can granulosa cells produce estrogens?

A

yes!

they have aromatase

113
Q

estrogens and progestins exert _______________________ on the anterior pituitary and hypothalamus depending on ________________

A

negative and positive feedback

the stage of the ovarian cycle

114
Q

Complete molar pregnancies

A

Tumor develops from tissue that forms after fertilization
Typically benign

115
Q

inhibin

A

negative feedback effect on the anterior pituitary

116
Q

the ovarian cycle is divided into

A

follicular and luteal phase

117
Q

Preeclampsia

A

Persistent high blood pressure during pregnancy

118
Q

follicular phase is marked by

A

increasing levels of estrogen

119
Q

the luteal phase is marked by

A

increased progesterone levels

120
Q

ovulation

A

transition period between follicular and luteal phase

121
Q

Preeclampsia is associated with

A

proteinuria

122
Q

estrogens are predominant _______________

progestins are predominant ______________

A

prior to ovulation

after ovulation

123
Q

Eclampsia

A

Preeclampsia + tonic-clonic seizures

124
Q

which hormone is increased largely right before ovulation?

A

LH

125
Q

Cure for preeclampsia

A

delivery of fetus and placenta

126
Q

during the late follicular phase and ovulation, what is going on with LH and estrogen?

A

high estrogen output
positive feedback of estrogen causes LH surge
surge of LH leads to ovulation

127
Q

Main symptom of preeclampsia

A

Edema

128
Q

during the early to mid luteal phase, what is going on?

A

decrease in LH causes rapid atrophy of corpus luteum

corpus lute secrets estrogen, progesterone and inhibin which inhibits release of gonadotropins (GnRH)

129
Q

Severe physical change during menopause

A

Osteoporosis and decreased bone strength

130
Q

during the late luteal phase, what is going on?

A

corpus luteum dies

decrease in estrogen, progesterone and inhibin

131
Q

Amenorrhea

A

Absence of menstruation or missed menstrual periods

132
Q

Most common cause of amenorrhea

A

Pregnancy

133
Q

Hormonal imbalances that can lead to amenorrhea

A

PCOS
Thyroid malfunction
Pituitary tumor
Premature menopause

134
Q

progesterone withdrawal causes

A

menstrual bleeding

135
Q

spinnbarkeit tests

A

ability of cervical mucus to stretch a distance before breaking

136
Q

Structural problems that can lead to amenorrhea

A

Uterine scarring
Lack of reproductive organs
Abnormal vagina

137
Q

ferning test

A

cervical mucus is collected on clean glass slide, allowed to dry
if it forms a pattern that resembles the fronds of a fern, the person is in ovulation

138
Q

Primary amenorrhea

A

Have not started period after puberty

139
Q

estrogen and progesterone hormonal contraceptives inhibit

A

LH, FSH, and GnRH secretion, preventing ovulation

140
Q

Secondary amenorrhea

A

Had normal periods that suddenly became absent

141
Q

additional role of progesterone in hormonal contraceptives

A

thickens cervical mucus to prevent passage of sperm into uterus

changes uterine lining to inhibit implantation

142
Q

Dysmenorrhea

A

pain accompanying menstruation
too much PGF2a (primary)
endometrial tissue outside uterus (secondary)

143
Q

Menorrhagia

A

excessive vaginal bleeding

144
Q

Metrorrhagia

A

irregular or overlong vaginal bleeding
bleeding/spotting between periods

145
Q

The ____ are most affected during primary amenorrhea

A

ovaries

146
Q

The ____ is least affected during primary amenorrhea

A

pituitary

147
Q

The ____ is most affected during secondary amenorrhea

A

hypothalamus

148
Q

The ____ is least affected during secondary amenorrhea

A

Uterus tract

149
Q

Polycystic ovary syndrome (PCOS)

A

Higher levels of male hormones, androgens, and type II diabetes more at risk

150
Q

Symptoms of PCOS

A

Menstrual irregularities
Cysts
Weight gain
Excess hair
Acne
Skin/mood changes

151
Q

Polycystic ovary cannot make

A

mature follicles
Follicles remain immature and eggs fail to be released regularly

152
Q

PCOS pathophys

A

Increased androgen and insulin are main players here

153
Q

Turner Syndrome (TS)

A

One copy of X chromosome is missing/altered in females

154
Q

Most common feature of TS

A

Short stature
Do not undergo puberty

Pathophysiology (18 decks)

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