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Reproductive > Physiology and pathology > Flashcards

Physiology and pathology Flashcards

1
Q

Primary oocyte

A

In fetal life–>meiosis I of prophase prior to ovulation

Diploid

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2
Q

What happens to the primary oocyte during Ovulation?

A

–>Meiosis II in metaphase II until fertilization

Haploid

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3
Q

How long does the oocyte have to fertilization before it degenerates?

A

1 day

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4
Q

Elevated hormones in ovulation

A

^estrogen–>^GnRH receptors on anterior pituitary–>^^^surge in LH–>rupture of the follicle

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5
Q

How does a spike in progesterone change basal temperature?

A

Temperature increases

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6
Q

Mittelschmerz

A

Transient mid-cycle ovulatory pain (peritoneal irritation) can mimic a appendicitis

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7
Q

Where does fertilization most commonly occur?

A

Ampulla of the fallopian tube

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8
Q

What secretes hCG?

A

Syncytiotrophoblasts (also stimulates the corpus luteum to make progesterone during the 1st trimester)

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9
Q

Suckling of the nipple stimulates?

A

Nerves to increase oxytocin and prolactin

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10
Q

Oxytocin function

A

Induces labor and stimulates milk let down

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11
Q

Prolactin function

A

Induces and maintains lactation and decreases reproductive function

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12
Q

What do breastfed infants require in addition?

A

Vitamin D

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13
Q

Function of the corpus luteum for the first 8-10 weeks?

A

Produce progesterone, functions as place holder until the placenta is large enough to make its own progesterone/estriol

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14
Q

Elevated hCG is indicative of?

A

Multiple gestations, hydatidiform moles, choriocarcinomas, Down syndrome

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15
Q

Decreased hCG is indicative of?

A

Edward, Patau, ectopic/failing pregnancy

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16
Q

What is the specific lab value indicating menopause?

A

FSH (loss of negative feedback from decreased estrogen)

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17
Q

Menopause before age 40 may indicate?

A

Premature ovarian failure

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18
Q

What are the hormonal changes associated with menopause?

A

Decrease in estrogen, Big increase in FSH, increase in LH and GnRH

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19
Q

Menopause symptoms

A 
Menopause wreaks HAVOCS
Hot flashes
Atrophy of the vagina
Osteoporosis
Coronary artery disease
Sleep disturbances
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20
Q

Where does spermatogenesis occur?

A

Seminiferous tubules

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21
Q

When does spermatogenesis begin?

A

At puberty

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22
Q

Spermatogonium ploidy

A

Diploid 2N, 2C (N=unique genetic content, C=cr)

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23
Q

Primary spermatocyte ploidy

A

Diploid 2N, 4C

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24
Q

Secondary spermatocyte ploidy

A

Haploid 1N (X or Y), 2C(XX or YY)

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25
Q

Spermatid ploidy

A

Haploid 1N, 1C

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26
Q

Mature spermatozoon

A

Haploid 1N, 1C (loss of cytoplasmic contents and gain of acrosomal cap

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27
Q

Androstenedione produced from?

A

ADrenals (AnDrostenedione)

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28
Q

Potency of androgens

A

DHT>testosterone>androstenedione

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29
Q

Main functions of testosterone

A

In utero: Develops the internal male structures

Puberty: Growth spurt, voice deepening, closing epiphyseal plates, libido

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30
Q

Main functions of DHT

A

In utero: Differentiation of external male structures

Later stage: Prostate growth, balding, sebaceous secretions

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31
Q

Effects of exogenous testosterone

A

Inhibitions Hypo-pit-gonadal axis–>decrease in intratestiscular testosterone–>azoospermia

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32
Q

Klinefelter syndrome presentation

A

Long limbs, testicular atrophy, Dev delay (maybe), female fat distribution/hair growth pattern

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33
Q

Klinefelter genotype and hormone levels

A

47, XXY
Dysgenesis of seminiferous tubules–>decrease in inhibin–>^FSH
Abnormal leydig function–>decrease in testosterone–>Increase in LH–>increase in estrogen

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34
Q

Turner syndrome genotype and hormone levels

A

45, XO
Decrease estrogen–>^FSH/LH
Can be monosomy or mosaic

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35
Q

Turner syndrome presentation

A

Webbed neck, cystic hygroma, shield chest, short stature, steak ovaries, preductal coarctation (Brachial>femoral pulse), bicuspid aortic valve

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36
Q

Rx for pregnancy in Turner syndrome

A

Oocyte donation with exogenous estradiol-17B and progesterone

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37
Q

Hormone levels in Kallman syndrome

A

Decreased GnRH, LH, FSH, testosterone–>infertility/amneorrhea

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38
Q

Kallman syndrome presentation

A

Failure to complete puberty, defect in GnRH cells and formation of olfactory bulb (anosmia)

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39
Q

Aromatase deficiency

A

Inability for females to synthesize estrogen from androgens–>masculinization of females

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40
Q

Female pseudo-hermaphrodite (XX)

A

Ovaries present, but external genitalia are virilized or ambiguous
Due to exogenous androgens or congential adrenal hyperplasia

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41
Q

Male pseudo-hermaphrodite (XY)

A

Testes present, but external genitalia are female

Due to androgen insensitivity syndrome

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42
Q

Testosterone and LH levels in: defective androgen receptor

A

Increase T and LH

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43
Q

Testosterone and LH levels in: Testosterone-secreting tumor

A

Increased T and decrease LH

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44
Q

Testosterone and LH levels in: Primary hypogonadism

A

Decreased T and increased LH

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45
Q

Testosterone and LH levels in: Hypogonadotropic hypogonadism

A

Decrease T and LH

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46
Q

Hydatidiform mole associated with

A

Theca-lutein cysts, hyperemesis gravidarum, hyperthyroid

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47
Q

Risk of cancer associated with moles?

A

2% risk of developed choriocarcinoma in COMPLETE moles

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48
Q

Symptoms of a complete mole

A

First trimester bleeding, enlarged uterus, hyperemesis, pre-eclampsia, hyperthyroidism

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49
Q

Imaging of a complete mole

A

Honey combed, grape clusters, snow storm on US

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50
Q

Symptoms of a partial mole

A

Vaginal bleeding and abdominal pain

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51
Q

Imaging of a partial mole

A

Fetal parts

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52
Q

Gestational HT presentation

A

BP>140/90 after 20th week of gestation
No pre-existing HT
No proteinuria or end organ damage

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53
Q

How do you treat gestational HT

A

Antihypertensives: a-methyldopa, labetalol, hydralazine, nifedipine
Deliver at 37-39 weeks

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54
Q

Preeclampsia presentation

A

New onset HT with proteinuria or end-organ dysfunction after 20th week of gestation

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55
Q

What are the causes of preeclampsia?

A

Abnormal placental spiral arteries–>endothelial dysfunction, vasoconstriction and ischemia

56
Q

Risk factors for preeclampsia

A

Pre-existing HT, diabetes, chronic renal dz, autoimmune disorders
Don’t give ACE I (renal damage!)

57
Q

How do you treat preeclampsia?

A

Antihypertensives, IV magnesium sulfate

Don’t give ACE I (renal damage!)

58
Q

Eclampsia presentation

A

Pre-eclampsia with seizures

Can lead to maternal death due to stroke, ICH, ARDS

59
Q

How do you treat eclampsia?

A

IV magnesium sulfate, antihypertensives, immediate delivery

60
Q

HELLP syndrome

A 
Hemolysis
Elevated liver enzymes
Low platelets
A manifestation of severe preeclampsia
Blood smear shows shistocytes
Can lead to hepatic subcapsular hematomas-->rupture-->severe hypotension
61
Q

Sheehan syndrome risk factors

A

No separation of the placenta after delivery–>postpartum bleeding–>necrosis of the anterior pituitary–>hypopituitarism

62
Q

Polyhydramnios is associated with

A

Fetal malformations (esophageal duodenal atresia, anencephaly–>can’t swallow fluid), maternal DM, fetal anemia, multiple gestations

63
Q

Oligohydramnios is associated with

A

Placental insufficiency, biltaeral renal agenesis, posterior urethral valves (males)–>can’t excrete urine
–>can lead to Potter sequence

64
Q

Incidence of gynecologic tumor embryology

A

Endometrial>ovarian>cervical

65
Q

Prognosis of gynecologic tumors

A

Ovarian>cervical>endometrial

66
Q

Sarcoma botryoides

A

Girls under 4 years
Spindle shaped cells, desmin+
Clear, grape-like polypoid mass emerging from vagina

67
Q

HPV 16 and 18 inhibit which genes

A

p53 suppressor gene (due to E6 gene product)

RB supressor gene (due to E7 gene product)

68
Q

Histology of cervical dysplasia

A

Koliocytes-wrinkled raisinoid nuclei

May have clearing or perinuclear halo

69
Q

Patients with polycystic ovarian syndrome are at risk for?

A

Endometrial cancer

70
Q

LH and FSH values in PCOS

A

3:1 LH/FSH–>activation of theca interna cells–>increase in androgens–> decreases the rate of follicular maturation and unruptured follicles become cysts

71
Q

PCOS presentation

A

Enlarged bilateral cystic ovaries
Amenorrhea/oligomenorrhea, hirsutism, acne, subfertility
Associated with obesity

72
Q

Theca-lutein cyst associated with

A

hydatiform mole and choriocarcinoma

73
Q

Theca-lutein cyst induced by

A

gonadotropin stimulation

74
Q

Follicular cyst induced by

A

hyperestrogenism, endometrial hyperplasia

75
Q

How do you monitor progression of Ovarian cancer?

A

CA-125

76
Q

Most common ovarian neoplasm

A

Serous cystadenoma

77
Q

What is it called when you see hyperthyroidism due to mature teratoma?

A

Struma ovvarii (functional thyroid tissue in the cyst)

78
Q

Call-exner bodies are associated with what type of cancer

A

Granulosa cell tumor

Granulosa cells haphazardly around collections of eosinophilic fluid, looks like primordial follicles

79
Q

Schiller-Duval bodies are associated with what type of cancer?

A

Yolk sac tumors

look like glomeruli

80
Q

Tumor marker associated with dysgerminoma

A

LDH+
hCG+
(fried egg cell appearance on histology)

81
Q

Tumor marker associated with yolk sac tumor

A

AFP+

82
Q

Leiomyoma

A

Most common tumor in females (^ in blacks, benign, E sen.)

Histology: whorled pattern of smooth muscle bundles with well demarcated borders

83
Q

How do you treat endometriosis

A

Rx. NSAIDs, OCPs, progestins, GnRH agonists, danazol, removal

84
Q

How do you treat endometritis?

A

Gentamicin+clindamycin with/without ampicillin

85
Q

Endometrial hyperplasia puts a patient at risk for?

A

Endometrial carcinoma

86
Q

Endometrial hyperplasia is typically caused by?

A

Elevated estrogen

87
Q

Endometrial hyperplasia presentation?

A

Postmenopausal bleeding

88
Q

Endometrial carcinoma presentation?

A

Vaginal bleeding (typically proceeded by endometrial hyperplasia)

89
Q

What is the most common gynecologic malignancy?

A

Endometrial carcinoma

90
Q

Endometrial carcinoma risk factors

A

Prolonged use of estrogen without progestins, obesity, diabetes, HT, nulliparity, later menopause, Lynch syndrome

91
Q

How do you treat lactational mastitis?

A

Dicloxacillin and continued breastfeeding

92
Q

When is male gynecomastia physiologic?

A

Birth, puberty, old age

93
Q

Drugs that induce gynecomastia?

A

Spironolactone, digoxin, cimetidine, alcohol, ketoconazle (seborrheic dermatitis)
Some drugs create awesome knockers

94
Q

What is the most important prognostic factor in malignant breast cancer?

A

Spread to the axillary nodes

95
Q

Risk factors for metastatic breast cancer

A

Increased estrogen exposure, ^ total number of menstrual cycles, older age at 1st live birth, obesity, BRCA1/BRCA2 mutation, African American ethnicity (increase risk of triple -)

96
Q

DCIS pathology

A

Fills ductal lumen, often see microcalcifications on mammography

97
Q

Comedocarcinoma

A

Subtype of DCIS with central necrosis

98
Q

Paget disease of the breast

A

Underlying DCIS or invasive cancer
Eczematous patches on nipples
Paget cells=large cells in epidermis with clear halo

99
Q

Orange peel breast skin is associated with?

A

Inflammatory malignant breast tumors

100
Q

Invasive ductal carcinoma

A

Firm, fibrous, rockhard mass, with shape margins with classic stellate infiltration on gross imaging

101
Q

Invasive ductal carcinoma histology

A

Small, glandular duct-like cells

102
Q

Invasive lobular carcinoma histology

A

Orderly rows of cells due to decreased E-cadherin expression

103
Q

Medullary breast cancer

A

Good prognosis

Fleshy, cellular, lymphocytic infiltrate

104
Q

Peyronie disease

A

“peyronie, curved like a pony”

fibrous plaque within tunica albuginea

105
Q

Where does prostatic adenocarcinoma arise

A

posterior prostate

106
Q

Where does the prostate most commonly metastasize to?

A

Bone

107
Q

Pulsatile leuprolide

A

GnRH agonist

108
Q

Continuous leuprolide

A

GnRH antagonist (decrease in FSH/LH)

109
Q

Clinical use of leuprolide

A 
Infertility (pulsatile)
Prostate cancer (continuous, use with flutamide)
Precocious puberty (continuous)
110
Q

Toxicity of leuprolide

A

Antiandrogen, nausea, vomitting

111
Q

Synthetic estrogen clinical use

A

Female hypogonadism, ovarian failure, menstural abnormalities, hormone replacement therapy,
Can be used in men with androgen-dependent prostate cancer

112
Q

Synthetic estrogen toxicity

A

Increased risk of endometrial cancer, bleeding in postmenopausal women, clear cell carcinoma of vagina in females exposed to DES in utero
Increased risk of thrombi
Contraindication in ER+ breast cancer and PH of DVTs

113
Q

Clomiphene mechanism

A

SERM: Antagonist at estrogen receptors in hypothalamus

Prevents normal feedback inhibition and increases release of LH and FSH from pituitary–>stimulates ovulation

114
Q

Clomiphene clinical use

A

Infertility (PCOS),

115
Q

Clomiphene toxicity

A

Hot flashes, ovarian enlargement multiple simultaneous pregnancies, visual disturbances

116
Q

Tamoxifen mechanism

A

Antagonist at breast, uterus

Agonist at bone

117
Q

Tamoxifen clinical use

A

Use to treat and prevent recurrence of ER/PR+ cancer

118
Q

Tamoxifen toxicity

A

Increases risk of thrombolytic events and endometrial cancer

119
Q

Raloxifene clinical use

A

Primarily used to treat osteoporosis

120
Q

Raloxifene toxicity

A

Increased risk of thromboembolic events but NO increased risk of endometrial cancer (like in tamoxifen)

121
Q

Raloxifene mechanism

A

Antagonist at breast, uterus

Agonist at bone

122
Q

Anastrozole/exemestane

A

Aromatase inhibitors use to postmenopausal women with ER+ breast cancer

123
Q

Progestins clinical use

A

bind progesterone receptors–>Decrease growth and increase vascularization of the endometrium

124
Q

Progestins clinical use

A

Oral contraceptives
Endometrial cancer Rx
Abnormal uterine bleeding

125
Q

Mifepristone mechanism

A

Competitive inhibitor of progestins at PR

126
Q

Mifepristone clinical use

A

Termination of pregnancy

127
Q

Mifepristone toxicity

A

Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain

128
Q

Terbutaline/ritodrine

A

B2 agonists: relax the uterus to decrease contraction frequency in women during labor

129
Q

Danazol mechanism

A

Partial adrogen agonist

130
Q

Danazol clinical use

A

Endometriosis, hereditary angioedema

131
Q

Danazol toxicity

A

“become like Dan (a man)”

Weight gain, edema, acne, hirsutism, masculinization, decrease HDL levels, hepatotoxicity

132
Q

Anti androgen names

A

Finasteride 5a-reductase inhibitor
Flutamide- Non steroidal competitive inhibitor at androgen receptors (prostate carcinoma)
Ketoconazole- Inhibits steroid synthesis
Spironolactone- Inhibits steroid binding

133
Q

Tamsulosin

A

A1-antagonist used to treat BPH (also terazosin)

Selevtive a1A,D receptors that are found on the prostate, not on vascular receptors (a1B)

134
Q

Sildenafil, vardenafil, tadalafil

A

Inhibits PDE-5–>^cGMP
Smooth muscle relaxation of corpus cavernosum
Increases blood flow to the penis
“FILl the penis”

135
Q

Sildenafil, vardenafil, tadalafil toxicity

A

HA, flushing, dyspepsia, cyanopsia (blue tinted vision)

**Risk of life threatening hyptotension in patients taking nitrates

136
Q

Minoxidil

A

Androgenetic alopecia, severe refractory hypertension

Direct arteriolar vasodilator

Reproductive (5 decks)

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