Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Repro > Flashcards

Repro Flashcards

1
Q

Pathogenesis of Klinefelters

A

Seminiferous tubule destruction and hyalinization -> small, firm testes; Leydig cell damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Klinefelters hormone levels

A

Serum inhibin low (S tubule dygenesis), low testosterone (Leydig dysfunction), high LH and FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cryptorchidism hormone levels

A

Seminiferous tubules dmg’d but NOT leydig cells; Low inhibin levels and high FSH lvls; but LH and testosterone levels normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Klinefelters clinical characteristics

A

Testicular atrophy, long extremities, gynecomastia, female hair distribution, presence of Barr bodies, mild ID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cells of seminiferous tubules and functions

A

Spermatogonia (germ cells) - produce primary spermatocytes. Sertoli cells (non-germ) - secrete inhibin (-| FSH), androgen-binding protein (maintain local testosterone lvl), blood-testis barrier (via tight junctions), support spermatozoa, produce MIF. Leydig cells (endocrine) - secrete testosterone in presence of LH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Temperature affects production of what in semineferous tubules?

A

Sertoli cells affected - decreased sperm production and decreased inhibin. Leydig cells NOT affected (testosterone levels okay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Three main categories of drugs for BPH?

A

Alpha-adrenergic antagonists (terazosin, tamsulosin), 5-alpha-reductase inhibitors (finasteride, dutasteride), antimuscarinics (tolterodine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Four possibilities when the urachus doesn’t obliterate

A

Patent urachus (urine from umbilicus), vesicourachal diverticulum (out pouching of bladder), urachal sinus (adj to umbilicus), urachal cyst (often asymptomatic but can be infectious, adenoca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sertoli v. Leydig. What makes MIF?

A

Sertoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fetal anomalies associated with polyhydramnios?

A

Anencephaly, GI atresia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Turner’s syndrome presentation

A

In neonate, lymphedema, cystic hygromas. Primary amenorrhea (streak ovaries), short statue, Coarctation of the aorta. Webbed neck, low hairline. Low estrogen, high LH and FSH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hydrocele

A

Serous fluid in tunica vaginalis. See fluid in sac. Communicating if processus vaginalis (diverticulum from peritoneum) remains patent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Complete mole vs. partial mole?

A

Complete - bleeding, enlarged uterus, PEC, Theca-lutein cysts, trophoblast only, no fetal tissue, 46 XX or XY (both paternal), with 15-20% risk of malignancy. Partial mole - bleeding, pain, fetus, cord, some enlarged villi, 69 XXX or XXY, with low risk malignancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Kallmann syndrome

A

Delayed pubery + anosmia. Etio - failure of GnRH-seceting neuron migration from olfactory placode to hypothalamus. Central hypogonadism and anosmia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Male gonadotropin regulation

A

Hypothalamus secretes GnRH pulsatile which POS pituitary. Pituitary releases FSH and LH (ant. pituitary). LH stimulates release of testosterone from Leydig, which negatively feedbacks to LH.. FSH stimulates release of inhibin B from sertoli, which negatively feedback for FSH. Lute for Leydig for L’testosterone. FSH to Sertoli to inhibin B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metabolic effects of human placental lactogen?

A

Increases insulin resistance, stimulates proteolysis and lipolysis, inhibits gluconeogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What control breast development during pregnancy?

A

1st TM - corpus produces progesterone and estradiol. By 2nd TM, placenta produces progesterone and estradiol, while fetal adrenal helps w/ estradiol. Prolactin increases (ant. pituitary) but is prevented from lactogenesis b/c of high estrogen and progesterone levels. Once placenta separates, prolactin stimulates milk production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Urge incontinence

A

Uninhibited bladder contractions (detrusor instability). M3 antagonists (e.g. oxybutynin) -> smooth muscle relaxation. (M3 is a Gq pathway, so drug dec. IP3 production).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sheehan’s syndrome

A

If significant hypotension occurs while pituitary is still enlarged (2/2 to high estrogen lvls, e.g. PPH) –> ischemic necrosis of pituitary –> panhypopituitarism -> prolactin deficiency for example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What day of separation leads to fetal membrane organization for monozygotic twins?

A

4,8,12. 4 Twins. FOUR is magic number. 0-4: di/di. 4-8:monochorionic/diamniotic; 8-12: mono/mono; >13: mono/mono conjoined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Histology changes in menstrual cycle

A

First half (proliferative phase). Estrogen stimulates proliferation of stratum FUNCTIONALE. Non-branching, non-budding EVENLY distributed. Tubular, narrow, pseudo stratified glands. Second half (secretory phase, begins with ovulation). Glands become LARGER and COILED w/ large vacuoles. Edematous stroma with SPIRAL arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Deformation vs. malformation vs disruption?

A

Deformation occurs due to extrinsic mechanical forces (e.g. Potter sequence). Disruption refers to secondary breakdown of previously normal tissue (amniotic band syndrome). Malformation is primary defect of cells (intrinsic developmental abnormality) (e.g. holoprosencephaly).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Koilocyte

A

Sign of infection with HPV. Immature squamous cell w/ dense, irregularly staining cytoplasm with PERINucLEAR clearing = halo. PYKNOTIC (apoptotic).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Parabasal cells

A

Round cells w/ HIGH N/C, basophilic cytoplasm. Dominate Pap smears of post-menopausal and postpartum women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ABO disease

A

Must be IgG ab’s (b/c only they cross placenta). Usually mothers make IgM uncless she is an O mom. Even so only 3% of O mom - X baby pregnancies have hemolytic disease of the newborn.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Achondroplasia

A

Constitutive activation (gain-of-function) of FGFR3. Sporadic mutation (adv. paternal age) in 85%, AD 15%. Homozygosity = death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Urethral trauma

A

Posterior urethral injury is associated with pelvic trauma while anterior urethral injury is associated with straddle injuries. Inability to void w/ full bladder, high-riding boggy prostate, blood at urethral meatus. NO FOLEY.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What contains the ovarian nerves, arteries, veins, and lymphatics?

A

Suspensory ligament of the ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment for hirsutism?

A

Spironolactone (blocks androgen receptors at hair follicles). Also flutamide (testosterone receptor antag) and finasteride (5-alpha-reductase inhibitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Vaginal adenosis?

A

Replacement of vaginal squamous epithelium with glandular columnar epithelium. Female children of women exposed to DES. Precursor to clear cell adenocarcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ambiguous external genitalia in female infant and maternal virilization?

A

Aromatase deficiency. AR. High androgen and low estrogen. Aromatase converts Androstenedione to estrone and testosterone to estradiol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tamoxifen

A

SERM that used for tx of osteoporosis and breast cancer. But associated with increased incidence of endometrial cancer and thromboembolic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Raloxifene

A

Also a SERM. Agonist on bone, CV, and blood lipoproteins. Antagonist to BREAST and UTERUS. Decreases incidence of breast cancer and osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Complete androgen insensitivity

A

Lack of androgen receptors in the body. 46,XY. Testosterone -> estradiol -> external female genitalia. Blind pouch vagina. Testes in the abdomen. Serum testosterone high, LH high, FSH normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Role of androgen binding protein (ABP)?

A

To ensure high lvls of testosterone in the seminiferous tubules to allow spermatogenesis to occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

PCOS hormones

A

LH thought to be high. Causing theca-cells to make lots of androgens and estrogens, suppressing FSH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Absolute contraindications to OCPs?

A

Prior hx of DVT/PE. Hx of estrogen-dependent rumor. Women > 35 who smoke heavily. HyperTG. Decompensated or active lier disease. Pregnancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Appendages in wrong locations?

A

Homeobox gnes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Gene involved in limb lengthening?

A

FGF gene. Produced at apical ectodermal ridge -> mitosis of underlying mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Gene mutation that can cause holoprosencephaly?

A

Sonic hedgehog gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Dorsal-ventral axis vs. anterior-posterior axis organization genes?

A

Shh (BASE) for ant-post. Wnt-6 (apical ectodermal ridge) for dorsal-ventral.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Bilaminar vs. trilaminar timeline?

A

2 weeks vs. 3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Morula timeline?

A

Day 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Implantation occurs when?

A

About 1 week after fertilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When do the genitalia differentiate?

A

Week 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When is fetal cardiac activity seen on US?

A

Week 6 (heart actually begins to beat at wk 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

When do the limb buds form?

A

Week 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mesodermal defect acronym?

A

VACTERL - Vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal defects, limb defects (bone and muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Thyroid embryo derivative?

A

Endoderm (follicular) and neural crest (parafollicular C cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Craniopharyngioma

A

Benign Rathke pouch (surface ectoderm) tumor with cholesterol crystals and calcifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Deformation vs. malformation?

A

Deformation is extrinsic occurring after “embryonic period,” whereas malformation is intrinsic (w 3-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Alkylating agent teratogenicity

A

Absence of digits, multiple anomalies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

ACEi teratogenicity

A

Renal damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Aminoglycosides teratogenicity

A

CN VIII tox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Carbamazepine teratogenicity

A

Neural tube, craniofacial, fingernail hypoplasia, dvpt delay, IUGR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

DES teratogenicity

A

Vaginal clear cell adnocarcinoma, congenital Mulerian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Folate antagonists teratogenicity

A

Neural tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Lithium teratogenicity

A

Ebstein anomaly (atrialized RV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Methimazole teratogenicity

A

Aplasia cutis congenita (congenital absence of skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Phenytoin teratogenicity

A

Fetal hydantoin syndrome = microcephaly, dysmorphic craniofacial, hypoplastic neails, cardiac, IUGR, intellectual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Thalidomide teratogenicity

A

Limb defects - phocomelia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Valproate teratogenicity

A

Neural tube defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Warfarin teratogenicity

A

Bone deformities, fetal emorrhage, abortion, optho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Cocaine teratogenicity

A

Abnormal fetal growth, fetal addiction, placental abruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Smoking teratogenicity

A

LOW birth rate. Preterm labor. Placental problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Iodine teratogenicity

A

Congenital goiter or hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Maternal diabetes teratogenicity

A

Caudal regression syndrome: anal atresia to sirenomelia; congenital heart, neural tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Vitamin A excess teratogenicity

A

Spontaneous abortions and birth defects (cleft palate, cardiac)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

X-ray teratogenicity

A

Microcephaly, ID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Fetal alcohol syndrome

A

ID, developmental retardation, microcephaly, holoprosencephaly, facial abnormalities (smooth philtrum, thin upper lib, small palpebral fissures, hyper telorism), limb dislocation, heart defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Cleavage at 0-4 days of monozygotic cell leads to

A

Fused OR separate placenta. But dichorionic diamniotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Cleavage at 4-8 days of monozygotic cell

A

Monochorionic, diamniotic (most common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Cleavage at 8-12 days of monozygotic cell

A

Monochorionic, monoamniotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Cleavage >13 days of monozygotic cel

A

Likely mono-mono but CONJOINED twins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Cytotrophobloast vs. Syncytiotrophobloast

A

cyto = inner layer of chorionic villi. Syncytio = outer layer that secretes hCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

When does the vitelline duct obliterate?

A

Week 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Aortic arch 1

A

Part of maxillary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Aortic arch 2

A

Stapedial artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Aortic arch 3

A

Common carotid arteries and beginning of internal carotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Aortic arch 4

A

Part of AA, part of right subclavian artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Aortic arch 6

A

Proximal part of pulmonary arteries and the ductus arterosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What do the branchial clefts do?

A

Branchial cleft 1 becomes external auditory meatus. Rest involute via temporary cervical sinus. If persist- > cyst in lateral neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Branchial arch 1 nerve and abnormality

A

Nerve is V3. Treacher Collins syndrome -> mandibular hypoplasia and facial abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Branchial arch 2 nerve and abnormality

A

Nerve is VII. Abnormality is congenital pharyngocutaneous fistula = fistula between tonsillar area and lateral neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Branchial arch 3 nerve

A

Nerve is IX.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Branchial arch 4-6 nerve

A

Nerve is X + recurrent X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Muscles of branchial arch 1

A

Muscles of mastication (temporalis, masseter, lateral and medial pterygoid, mylohyoid), ant. belly of digastric, tensor tympani, tensor veli palatini

88
Q

Muscles of branchial arch 2

A

Facial expression, Stapedius, Stylohyoid, platysma, and post. belly of digastric

89
Q

Muscles of branchial arch 3

A

Stylopharyngeus

90
Q

Muscles of branchial arches 4,6

A

Pharyngeal, laryngeal

91
Q

Cartilages of branchial arch 1

A

Meckel cartilage: Mandible, Malleus, incus, spheno-mandibular ligament

92
Q

Cartilages of branchial arch 2

A

Stapes, sytloid process, lesser horn of hyoid, stylohyoid

93
Q

Cartilage of branchial arch 3

A

Greater horn of the hyoid

94
Q

Cartilages of 4,6th branchial arch

A

Thyroid, cricoid, arytenoids, croniculate, cuneiform

95
Q

Branchial pouch 1

A

Middle ear, eustachian tube, mastoid air cells. ENDODERM

96
Q

Branchial pouch 2

A

Epithelial lining of palatine tonsil

97
Q

Branchial pouch 3

A

Dorsal - inferior parathyroid. Ventral - thymus.

98
Q

Branchial pouch 4

A

Dorsal - superior parathyroids. Ventral - C-cells of thyroid gland.

99
Q

Two mechanisms for cleft palate

A

Failure to fuse 2 lateral palatine processes. Fusion of one or more lateral palatine processes with the nasal septum and/or median palatine process

100
Q

Cleft lip mech

A

Failure of fusion of maxillary and medial NASAL processes

101
Q

Other names of Mullerian and Wolffian ducts?

A

Mullerian = parameonephric. Wolffian = mesonephric (renal)

102
Q

Components of the Wolffian duct

A

SEED (Seminal vesicles, epididymis, ejaculatory duct, ductus deferens). NOT prostate.

103
Q

What internal and external genitalia result in a XY has no MIF working?

A

Both male AND female internal genitalia. But male external genitalia (DHT going strong)

104
Q

What internal and external genitalia results in a XY with 5alpha reductase deficiency?

A

Male internal genitalia but ambiguous external genitalia until puberty

105
Q

Homolog of scrotum?

A

Labia majora

106
Q

Homolog of Prostate gland?

A

Urethral and paraurethral glands of Skene

107
Q

Homolog of Bartholin gland?

A

Bublourethral glands of Cowper

108
Q

Homolog of Corpus cavernous and spongiosum?

A

Vestibular bulbs

109
Q

Homolog of the labia minor?

A

Ventral shaft of penis

110
Q

Hypospadia vs. epispadia

A

Ventral vs. dorsal. Failure to close fold vs. faulty positioning of genital tubercle.

111
Q

Processus vaginalis

A

It is an evagination of the peritoneum that forms the tunica vaginalis in men and obliterates in women.

112
Q

Gubernaculum?

A

The anchor that brings down the testes during its descent OR what becomes the ovarian ligament and round ligament of the uterus

113
Q

What’s weird about the venous drainage of the gonads?

A

The left side always goes from L gonadal vein into the L renal vein to IVC, whereas the R gonadal vein goes directly into the IVC.

114
Q

Where are the uterine vessels located?

A

In the cardinal ligament. (Cervix to side wall of pelvis). Be careful of the ureters

115
Q

Where are the ovarian vessels located?

A

Suspensory ligament of the ovaries. Be careful of the ureters.

116
Q

Broad ligament contains what?

A

Ovaries, fallopian tubes, round ligament of the uterus

117
Q

Round ligament connects what?

A

Uterine fundus to the labia major. (Round ligament pain)

118
Q

Ovarian ligament connects what?

A

Medial pole of the ovary to the lateral uterus. Not in the broad ligament.

119
Q

Histology of the female reproductive tract.

A

Stratified epithelium from vagina to transformation jone. Now simple columnar epithelium up into fallopian tubes. Ovaries have simple cuboidal epithelium on the outer surface.

120
Q

Pathway of sperm?

A

Seminiferous tubules, Epididymis, Vas deferens, Ejaculatory ducts, (Nothing), Urethra, Penis. SEVEN UP.

121
Q

Physiology of erection

A

PNS (pelvic). NO leads to increased cGMP -> SMC RELAX = blood filling. With sympathetic tone, NE -> increased Ca2+ which leads to SMC contraction and vasoconstriction = flaccid.

122
Q

What nerves responsible for “shoot?”

A

SNS’ hypogastric n. for emission. Pudendal nerve for ejaculation.

123
Q

Theca cell role?

A

Desmolase converts cholesterol into androstenedione.

124
Q

Granulosa cell role

A

Aromatase converts androstendeione from theca cells into estrogen.

125
Q

Potency of estrogen-family hormones?

A

Estradiol (ovary) > estrone (peripheral) > estriol (placenta), which btw, is an indicator for fetal well being

126
Q

What makes progesterone?

A

Corpus luteum, placenta, adrenal gland, testes

127
Q

Function of progesterone

A

Endometrial glandular secretion, spinal artery development, maintain pregnancy, dec. myometrial excitability, thick cervical mucus to inhibit sperm entry, inhibits LH, FSH, uterine smooth muscle relaxation, dec. estrogen receptor expressivity, prevents endometrial hyperplasia

128
Q

Tanner II vs. III vs IV

A

II is pubarche and telarche. III is darkening, curling, enlargement. But IV has darker scrotal skin, development of the glans, and raised areolae

129
Q

Arrested development of oocytes where?

A

Meiosis is begun in fetal life but stops at Prophase 1 until selected for ovulation. As primary oocyte, finishes meiosis I and becomes secondary oocyte. It is arrested in METAphase II until fertilization. Must fertilize within ONE day.

130
Q

Mittelschmerz

A

Transient mid-cycle ovulatory pain classicularlly associated with peritoneal irritation.

131
Q

Exclusively breast fed infants require what vitamin supplementation?

A

Vitamin D

132
Q

hCG role

A

Made by syncytiotrophoblast and acts like LH in 1st TM, which is required for the luteal cell to continue making progesterone (maintaining the pregnancy). In 2nd-3rd TM, corpus luteum degenerates.

133
Q

hCG subunit for pregnancy test?

A

Beta subunit b/c alpha subunit is identical to LH, FSH, and TSH.

134
Q

How to diagnosis menopause?

A

FSH increased (very specific)

135
Q

Symptoms of menopause?

A

HAVOCS - Hot flashes, atrophy of the vagina, osteoporosis, coronary artery disease, sleep disturbances

136
Q

How long does spermatogenesis take?

A

2 months

137
Q

Spermatogonia vs. spertazooa?

A

Going to tbe a pserm. Zooa have acrosomal cap and loss of cytoplasm = zooming.

138
Q

Potency of androgens?

A

DHT > tesosterone > androstenedione

139
Q

Where do androgens get converted into estrogens in men?

A

Adipose and testis (Cytochrome P-450 aromatase)

140
Q

Function of DHT?

A

Early on, in differentiation of male external genitalia plus prostate. Late - involved in prostate growth, balding, sebaceous gland activity

141
Q

Function of testosterone

A

Differentiation of epididymis, vas, seminal vesicles. Growth spurt. Voice deepening. Closure of epiphyseal plates. Libido.

142
Q

XYY Presentation

A

Pheno normal. Tall, acne, antisocial in 1-2%. Normal fertility.

143
Q

Men: Testosterone down, LH down?

A

Hypogonadotropic hypogonadism

144
Q

Men: Testosterone down, LH up?

A

Primary hypogonadism

145
Q

Men: Testosterone up, LH down?

A

Exogenous testosterone (tumor, drugs)

146
Q

Men: Testosterone up, LH up?

A

Androgen receptor defect

147
Q

Most common etiology of a male pseudohermaphrodite?

A

Androgen insensitivity syndrome. Testes present but external genitalia are female/ambiguous.

148
Q

Most common etiology of a female pseudohermaphrodite?

A

Congenital adrenal hyperpasia or exogenous androgens during pregnancy. Ovaries present but virilized/ambiguous external genitalia.

149
Q

Aromatase deficiency

A

Can’t make estrogens from androgens -> masculization of females (ambiguous genitalia) +/- maternal virilization during pregnancy because fetal androgens cross the placenta. Increased serum testosterone and androstenedione.

150
Q

Androgen insensitivity syndrome

A

46 XY that is a normal appearing female with female external genitalia with rudimentary vagina. NO uterus or fallopian tubes. Testes (often found in labia majora). Increased testosterone, estrogen, and LH.

151
Q

5alpha-reductase deficiency

A

AR and only limited in phenotype to males. Inability to convert testosterone -> DHT means ambiguous genitalia until puberty when increased testosterone -> masculinization and growth of external genitalia. NORMAL testosterone/estrogen. LH normal or increased. Internal genitalia are normal.

152
Q

Kallmann syndrome

A

Hypogonadtropic hypogonadism 2/2 defect of GnRH migration. Decreased GnRH, decreased FSH, LH, testosterone, infertility. Anosmia.

153
Q

Etiology of complete vs. partial mole?

A

Complete mole is completely paternal (which duplicates its genome) + enucleated egg. Partial mole = 2 sperm + egg.

154
Q

Week cut-off for diagnosing gestational HTN?

A

Wk 20. HTN before week 20 suggests a molar pregnancy.

155
Q

Treatment for gestational HTN?

A

alpha-methyldopa, labetalol, hydralazine, nefidipine; delivery at 39 weeks

156
Q

Preeclampsia?

A

HTN > 20th week + proteinuria (>300 mg/24h). Severe features are Bp > 160/110, end-rgan damage. Caused by ABNL Spiral Arteries -> maternal endothelial dysf(x), vasoconstriction, and hyperreflexia

157
Q

HELLP syndrome?

A

Hemolysis, elevated liver (enzymes), Low platelet count. Tx = immediate delivery

158
Q

Tx differences between pre-eclampsia and eclampsia?

A

Both give antihypertensives, IV MgSO4. But immediately deliver in ecclampsia b/c of risk of maternal death 2/2 stroke w/ intracranial hemorrhage or ARDS

159
Q

Increased incidence of PEC found with what conditions?

A

Pre-exisitng HTN, DM, chronic renal disease, or autoimmune disorders

160
Q

Abnormal placental detachment types?

A

Placenta accreta attaches to myometrium w/o penetrating. Placenta increta penetrates into myometrium. Placenta percreta penetrates into uterine seroa —> rectal or bladder attachment.

161
Q

Presentation of placental abruption?

A

Abrupt, painful bleeding (concealed or apparent) in 3rd TM. Maternal DIC, shock, fetal distress.

162
Q

Placenta previa

A

Attachment of placenta near the cervical os -> inc. risk of bleeding. RF’s = multiparty, prior C-section

163
Q

Presentation of ectopic pregnancy?

A

Sudden lower abdominal pain w/ or w/o vaginal bleeding. Amenorrhea. Lower-than-expected bCG rise. r/o appi. US diagnosis.

164
Q

Pathophysiology of HPV virus -> cervical carcinoma?

A

HPV 16 and 18 produce two proteins: E6 and E7. E6 inhibits p53 while E7 inhibits RB. The virus, therefore, inhibits tumor suppressor genes

165
Q

Endometritis inflammatory picture? What cells?

A

Plasma cells and lymphocytes.

166
Q

Treatment of endometriosis?

A

NSAIDs, OCPs, progestins, GnRH agonists, surgery.

167
Q

Adenomyosis

A

Extension of endometrial tissue into the myometrium. Presents with dysmenorrhea, menorrhagia. ENLARGED, soft uterus. Tx = hysterectomy.

168
Q

RF’s for endometrial hyperplasia?

A

Anovulatory cycles, HRT, PCOS, granulosa cell tumor.

169
Q

Peak occurrence of leiomyomas?

A

Age 20-40

170
Q

Most common causes of an ovulation?

A

Pregnancy, PCOS, obesity, HPO axis, premature ovarian failure, hyperprolactinemia, thyroid, eating

171
Q

PCOS labs?

A

High androgens, High LH, low FSH. High androgens decrease SHBG -> increased FREE testosterone (active portion).

172
Q

Mechanism for OCP treatment for PCOS?

A

Estrogens increase SHBG -> decreased free testosterone

173
Q

Complications of PCOS?

A

Increased risk of endometrial cancer b/c of increased estrogens and absence of progesterone. (Therefore, tx with progesterones)

174
Q

Most common ovarian mass in young women?

A

Follicular cyst

175
Q

Cyst associated with choriocarcinoma and moles?

A

Theca-lutein cyst

176
Q

“Chocolate cyst”

A

Endometriosis. Blood gives it the color.

177
Q

Dermoid cyst

A

Mature teratoma with all sorts of tissue.

178
Q

Corpus luteum cyst

A

2/2 hemorrhage into a persistent corpus luteum. Self-resolves.

179
Q

Follicular cyst

A

Distention of unruptured graafian follicle. Often associated with hyperestrogenism and endometrial hyperplasia.

180
Q

Most common ovarian neoplasm?

A

Serous cystadenoma - benign. Thin0walled. Fallopian-like epithelium.

181
Q

Immature vs. mature teratoma?

A

Immature teratoma is malignant. More likely to contain thyroid tissue +/- embryonic-like neural tissue.

182
Q

Psammomma bodied malignant ovarian neoplasm?

A

Serous cystadenocarcinoma

183
Q

Granulosa cell tumor

A

Most common sex-cord tumor. Often produce estrogen/progesterone, so pt’s present with abnormal uterine bleeding or sexual precocity. Call-Exner bodies.

184
Q

Vaginal clear cell adenocarcinoma?

A

Women who had DES exposure in utero

185
Q

Small, mobile firm breast mass that increases in size and tenderness right before menstruation?

A

Fibroadenoma - found in stroma

186
Q

Serous or bloody nipple discharge?

A

Intraductal papilloma. Typically grows beneath areola (lactiferous sinus) and has a slight 1.5-2x risk of carcinoma.

187
Q

Phyllodes tumor?

A

LARGE bulky mass of connective tissue (stroma). “Leaf-like” 6th decade

188
Q

Non-invasive breast neoplasms?

A

DCIS (doesn’t penetrate BM; in major duct), Comedocarcinoma (caseous necrosis; type of DCIS), Paget disease of breast (results from underlying DCIS extending up to lactiferous ducts).

189
Q

Invasive ductal vs. invasive lobular breast cancer?

A

Ductal is worst, most invasive. Firm, “rock-hard” with sharp margins. Stellate infiltration. Invasive lobular is an ORDELRY row (“Indian file”)

190
Q

Acute mastitis?

A

An abscess. Staph aureus is most common. Tx = dicloxacillin + continued breast feeding

191
Q

Drugs that can cause gynecomastia?

A

Spironolactone, marijuana, digitalis, estrogen, cimetidine, alcohol, heroin, dopamine D2 antagonists, ketoconazole

192
Q

What lobes enlarge in BPH?

A

Lateral and middle

193
Q

What lobes enlarge in prostatic adenocarcinoma?

A

Posterior lobe

194
Q

Treatment of BPH?

A

alpha-1-antagonists (tamsulosin, terazosin). Finasteride (5-alpha reductase inhibitor)

195
Q

Etiology of variocele?

A

Poor gonadal venous drainage. Usu. left b/c -> L renal vein.

196
Q

Presentation of variocele?

A

Scrotal enlargement, bag of worms, dx w/ US. Decreases fertility b/c of increased temperature (Sertoli cell sensitive)

197
Q

Non-tranilluminating testicular mass

A

Cancer

198
Q

Seminoma

A

Painless homogenous testicular enlargement in 3rd decade. “Fried egg” on histo. Increased placental alkaline phosphate. Good prognosis. Tx = radiation (sensitive)

199
Q

Most common testicular tumor of boys < 3 y/o

A

Yolk sac (endodermal sinus) tumor. “Schiller-Duval bodies’

200
Q

GnRH analog?

A

Leuprolide

201
Q

Clinical uses of leuprolide?

A

Pulsatile dosages used for infertility. Continuous uses used for uterine fibroids, precocious puberty, and prostate ca (with flutamide).

202
Q

Names of estrogen drugs

A

Ethinyl estradiol, DES, mestranol

203
Q

Clinical use of estrogens

A

Hypogonadism/ovarian failure, menstrual abnormalities, HRT, men with androgen-dependent prostate cancer

204
Q

Clomiphene

A

Antagonist of estrogen receptors in hypothalamus preventing normal feedback inhibition -> increased LH and FSH. Used to treat infertility due to anovulation. SE’s - hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances

205
Q

Tamoxifen vs. raloxifene

A

Tamoxifen is antagonist on breast, agonist for uterus and bone. Raloxifene is agonist to bone, antagonist for uterus. Both associated with DVTs. Tamoxifen for breast cancer, raloxifene for osteoporosis.

206
Q

Aromatase inhibitors?

A

Used for breast cancer. Anastrozole/exemestane

207
Q

Mifepristone

A

Competetive inhibitor of progestins. Used with misoprostol (PGE1) for abortion.

208
Q

Mechanisms of estrogen/progestin vs progestin-only OCPS?

A

Progestin only causes thickening of cervical mucus and inhibits endometrial proliferation. E/P’s inhibit LH/FSH to prevent ovulation.

209
Q

Terbutaline

A

A beta-2 agonist used as a tocolytic in labor.

210
Q

Danazol

A

Partial agonist for androgen receptors. Used for endometriosis and hereditary angioedema.

211
Q

Finasteride

A

5 alpha-reductase inhibitor. Used for BPH and male pattern baldness.

212
Q

Flutamide

A

Competetive inhibitor of androgens at testosterone receptor used for prostate carcinoma.

213
Q

17,20 desmolase inhibitors

A

Ketoconazole and spironolactone (also inhibits 17-alpha hydroxylase). Both used for PCOS to prevent hirsuitism. Side effects of gynecomastia and amenorrhea.

214
Q

Side effects of PDE5 inhibitors?

A

HA, flushing, dyspepsia, color-vision. Hypotension if used with nitrates = life-threatening

215
Q

Role of menotropin in fertility treatment?

A

Menotropin acts like FSH –> formation of dominant follicle. hCG is then used for LH surge to ovulate.

216
Q

Primary energy source for sperm?

A

Fructose. Therefore relies on aldose reductase (glucose to sorbitol) and sorbitol dehydrogenase (sorbitol to fructose). High sorbitol dehydrognease activity.

Step 1 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions