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USMLE STEP 1 > Reproduction > Flashcards

Reproduction Flashcards

1
Q 
Sonic Hedgehog Gene
Where is it produced?
What axis does it pattern?
Involved with the development of what system??
Mutations lead to
A

Produced at base of limbs in zones of polarizing activity
Anterior Posterior Axis
Involved in CNS development
Mutations –> holoprosencephaly

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2
Q

Wnt 7 gene
Where is it produced?
What axis does it pattern?

A

Produced at apical ectodermal ridge (thickened ectoderm at distal end of each developing limb)
Dorsal Ventral Axis

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3
Q

FGF Gene
Where is it produced?
What does it do?

A

Produced at apical ectodermal ridge

Stimulates mitosis of underlying mesoderm, providing for lengthening limbs

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4
Q

Homeobox (Hox) Genes
What dos it do?
What axis?
Mutations result in

A

Involved in segmental organization of embryo in craniocaudal direction
Hox mutations –> appendages in wrong location

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5
Q

Day 0

A

Fertilization by sperm forms zygote initiating embryogenesis

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6
Q

Week 1

A

hCG secretion begins after implantation of blastocyst

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7
Q

Week 2

A

“2 weeks = 2 layers”

Bilaminar disc with epiblast and hypoblast

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8
Q

Week 3

A

3 weeks = 3 layers
Trilaminar disc
Gastrulation
Primitive streak, notochord, mesoderm and its organization, and neural plate begins to form

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9
Q

Week 3 - week 8
By week 4
Danger?

A 
Embryonic Period
Neural tube formed by neuroectoderm and closes by week 4
Heart begins to beat at week 4
4 weeks = 4 limbs 
upper and lower limb buds begin to form
Organogenesis
Extremely susceptible to teratogens
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10
Q

Week 8

A

Start of fetal period

Fetal movement and fetus looks like a baby

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11
Q

Week 10

A

Genitalia have male/female characteristics

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12
Q

Gastrulation
What is established?
Starts with…

A

Process that forms the trilaminar disc
Establishes ectoderm, endoderm and mesoderm
Starts with epiblast invaginating to form primitive streak

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13
Q

What comes from Surface Ectoderm?

A

Adenohypophysis (Ant Pituitary from Rathke’s Pouch), Lens, Epithelial lining of oral cavity, Sensory organ of ear, Anal canal below pectinate line, Parotid, Sweat, and Mammary glands

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14
Q

What comes from Neuroectoderm?

A

Brain (neurohypophysis, CNS neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland)
Retina, Optic Nerve, Spinal Cord

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15
Q

What comes from Neural Crest Cells?

A

PNS (DRG, CN, Celiac ganglion, Schwann cells, ANS)
Melanocytes, Chromaffin Cells of adrenal medulla, Parafollicular (C) cells of thyroid, Schwann cells, Pia and Arachnoid, Bones of skull, Odontoblasts, Aorticopulmonary septum

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16
Q

Craniopharyngioma
Origin
Histo

A

Benign Rathke’s pouch rumor with cholesterol crystals and calcification

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17
Q

What comes from Mesoderm?

A

Muscle, Bone, Connective Tissue, Serous Lining of Body Cavities (Peritoneum), Spleen, CV Structures, Lymphatics, Blood, Wall of Gut Tube, Wall of Bladder, Urethra, Vagina, Kidneys, Adrenal Cortex, Dermis, Testes, Ovaries

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18
Q

Mesodermal Defects

A 
"VACTERL"
Vertebral defects
Anal atresia
Cardiac defects
Tracheo-Esophageal fistula
Renal defects
Limb defects (bone and muscle)
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19
Q

What comes from Endoderm?

A

Gut tube epithelium (including anal canal above pectinate line)
Luminal epithelium derivatives (Liver, Lung, Gallbladder, Pancreas, Eustachian Tube, Thymus, Parathyroid, Thyroid follicular cells

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20
Q

Agenesis

A

Absent organ due to absent primordial tissue

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21
Q

Aplasia

A

Absent organ despite presence of primordial tissue

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22
Q

Deformation

A

Extrinsic disruption

Occurs after embryonic period

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23
Q

Hypoplasia

A

Incomplete organ development

Primordial tissue present

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24
Q

Malformation

A

Intrinsic disruption

Occurs during embryonic period (3-8 weeks)

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25
Q

Teratogenic Effects of ACEI

A

Renal damage

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26
Q

Teratogenic Effects of Alkylating Agents

A

Absence of digits

Multiple abnormalities

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27
Q

Teratogenic Effects of Aminoglycosides

A

“A mean guy hit the baby in the ear”

CN VIII toxicity

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28
Q

Teratogenic Effects of Carbamazepine

A 
Neural tube defects 
Craniofacial defects
Fingernail hypoplasia
Developmental delay
IUGR (IntraUterine Growth Restriction )
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29
Q

Teratogenic Effects of Diethylstilbestrol (DES)

A

Vaginal clear cell carcinoma

Congenital Mullerian anomalies

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30
Q

Teratogenic Effects of Folate Antagonists

A

Neural Tube Defects

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31
Q

Teratogenic Effects of Li

A

Ebstein’s Anomaly (Atrialized RV)

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32
Q

Teratogenic Effects of Phenytoin

A

Fetal hydantoin syndrome: microcephaly, dysmorphic craniofacial features, hypoplastic nails and distal phalanges, cardiac defects, IUGR (IntraUterine Growth Restriction ), mental retardation

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33
Q

Teratogenic Effects of Tetracyclines

A

Discolored Teeth

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34
Q

Teratogenic Effects of Valproate

A

Inhibition of maternal folate absorption –> neural tube defects

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35
Q

Teratogenic Effects of Warfarin

A

“Do not wage Warfare on the baby, keep in Heppy with Heparin (does not cross the placenta)”

Bone deformities, fetal hemorrhage, abortion, ophthalmologic abnormalities

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36
Q

Teratogenic Effects of Thalidomide

A 
"Limb Defects with tha-LIMB-domide"
Limb defects (flipper limbs)
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37
Q

Teratogenic Effects of EtOH

A

Leading cause of birth defects and mental retardation

Fetal Alcohol Syndrome

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38
Q

Teratogenic Effects of Cocaine

A

Abnormal fetal development and fetal addiction; Placenta abruption

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39
Q

Teratogenic Effects of Smoking (nicotine, CO)

A

Preterm labor, Placental problems, IUGR (IntraUterine Growth Restriction ), ADHD

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40
Q

Teratogenic Effects of Iodide (Lack or Excess)

A

Congenital Goiter or Hypothyroidism (cretinism)

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41
Q

Teratogenic Effects of Maternal Diabetes

A

Caudal regression syndrome (anal atresia to sirenomelia), Congenital Heart Defects (Transposition of the Great Vessels), Neural Tube Defects

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42
Q

Teratogenic Effects of Excess Vit A

A

Extremely high risk for spontaneous abortions and birth defects (cleft palate, cardiac abnormalities)

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43
Q

Teratogenic Effects of X Rays

A

Microcephaly, Mental Retardation

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44
Q

Fetal Alcohol Syndrome

A

Mental Retardation, Pre and Post Natal Developmental Retardation, Microcephaly, Holoprosencephaly, Facial Abnormalities, Limb Dislocation, Heart and Lung Fistulas

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45
Q

Source of Estrogen

A

Ovary –> 17β-estradiol
Placenta –> estriol
Adipose tissue –> estrone via aromatization

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46
Q

Potency of different kinds of estrogens

A

Estradiol > Estrone > Estiol

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47
Q 
Estrogen Function 
Development
In menstrual cycle 
Receptors 
Blood
A

Development of genitalia, breast, and female fat distribution
Growth of follicle, endometrial proliferation, and ↑ myometrial excitability
Feedback inhibition of LH and FSH and then LH surge
Stimulation of prolactin secretion (but blocks it’s action at the breast)
Upregulates estrogen, LH, and progesterone receptors
↑ Transport proteins, SHBG, HDL, ↓LDL

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48
Q

How does pregnancy change estrogen levels

A

50x ↑ in estradiol and estrone

1000x ↑ in estiol (indicator of fetal well being

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49
Q

Mechanism of estrogen receptor

A

Expressed in cytoplasm

When bound with ligand, translocates to the nucleus

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50
Q

Molecular cascade in Theca Cells

A

Pulsatile GnRH –> LH –> Desmolase

D turns cholesterol in to androstenedione

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51
Q

Molecular cascade in Granulosa Cells

A

Pulsatile GnRH –> FSH –> Aromatase

A turns androstenedione into estrogen

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52
Q

Source of Progesterone

A

Corpus Luteum, Placenta, Adrenal Cortex, Testes

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53
Q

Elevation of Progesterone indicates…

A

Ovulation

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54
Q

Function of Progesterone
Menstural cycle
Receptors
Pregnancy

A

Stimulation of endometrial glandular secretions and spiral artery development
Maintains endometrium to support implantation
–/ LH and FSH
↓ myometrial excitability
↓ estrogen receptor expressivity
Maintain pregnancy
Production of thick cervical mucus (inhibits sperm entry into uterus)
↑ Body Temp
Uterine smooth muscle relaxation (prevents contractions)

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55
Q

Tanner Stages of Sexual Development

A

I: Childhood
II: Pubic hair appears (Pubarche), Breast bud forms (Thelarche)
III: Pubic hair darkens and becomes curly. Penis size/length and breasts enlarge
IV: Penis width ↑, Darker scrotal skin, Development of glans, raised areolae
V: Adult. Areolae are no longer raised

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56
Q 
Follicular Phase 
Estrogen
FSH
LH
Progesterone
A

Estrogen: Stead rise
FSH: Rises slightly then decreases slightly
LH: Rises slightly then decreases slightly
Progesterone: Low

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57
Q 
Luteal Phase 
Estrogen
FSH
LH
Progesterone
A

Estrogen: decreases, then spikes briefly before decreasing again
FSH low
LH low
Progesterone: increases then decreases

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58
Q 
Ovulation
Estrogen
FSH
LH
Progesterone
GnRH
Temp
A 
Estrogen: just past peak
FSH: low surge
LH: high surge
Progesterone: beginning to rise 
↑ in GnRH receptors on ant pituitary
↑ Temp (due to progesterone)
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59
Q

Basic schematic of menstrual cycle

A

↑ estrogen –> LH surge –> Ovulation –> Progesterone (from corpus luteum) –> Progesterone levels fall –> menstruation (apoptosis of endometrial cells)

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60
Q

Length of Follicular phase

A

Variable

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61
Q

Length of Luteal phase

A

Constant 14 days

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62
Q

When is follicular growth fastest?

A

2nd week of proliferative phase (follicular phase)

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63
Q

Oligomenorrhea

A

Cycle > 35 days

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64
Q

Polymenorrhea

A

Cycle < 21 days

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65
Q

Menometrorrhagia

A

Heavy, irregular menstruation at irregular intervals

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66
Q

Mittelschmerz

A

Blood from ruptured follicle or follicular enlargement causes peritoneal irritation that can mimic appendicitis

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67
Q

Primary Oocytes
N
C
When do they enter and complete meiosis I

A

2N 4C

Begin meiosis I during fetal life and complete meiosis I just prior to ovulation

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68
Q

When is meiosis II arrested?

Until when?

A

“Arrested until egg MET sperm”

Meiosis II arrested at Metaphase II until fertilization

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69
Q

If fertilization does not occur within 1 day what happens to secondary oocytes?

A

Degenerate

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70
Q

Oogenesis

Names of cells with N and C

A

Oogonium (2N 2C) –> Primary Oocyte (2N 4C) –> Secondary Oocyte (1N 2C) –> Ovum (1N 1C)

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71
Q

Where and When does fertilization most commonly occur?

A

Upper end of fallopian tube (ampulla) within 1 day of ovulation

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72
Q

When does implantation within the wall of the uterus occur?

A

Within 6 days after fertilization

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73
Q

What secretes hCG?

When is hCG first detectable in blood and urine?

A

Trophoblast secretes hCG
Detectable in blood 1 week after conception
Detectable in urine 2 weeks after conception

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74
Q

Lactation
When does it occur?
What has changed chemically that allows it to happen?
What is required to maintain lactation?

A

Occurs after labor because progesterone ↓ and this allows lactation to occur
Suckling is required to maintain lactation: ↑ nerve stimulation –> ↑ oxytocin and prolactin

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75
Q

Prolactin

What does it do?

A

Induces and maintains lactation and ↓ reproductive function

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76
Q

Oxytocin

What does it do?

A

Helps with milk letdown and involved with uterine contraction

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77
Q

hCG
Source
Function
Uses

A

Syncytiotrophoblast of placenta
Maintains corpus luteum (and thus progesterone) for 1st trimester by acting like LH
Used to detect pregnancy

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78
Q

Why is hCG not needed in 2nd and 3rd trimesters?

A

Placenta synthesizes its own estriol and progesterone

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79
Q

Elevated hCG in pathological states

A

Hydatidiform moles, choriocarcinoma

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80
Q

Average age of menopause?

What makes it earlier?

A

Average age at onset is 51

Earlier in smokers

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81
Q

What is happening hormonally in menopause?

A

↓ estrogen production becuse of ↓ # of follicles
↑↑FSH, ↑LH (no surge), ↑GnRH
Ovaries continue to produce androgens under LH stimulation

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82
Q

What usually precedes menopause?

A

4-5 years of abnormal menstrual cycles

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83
Q

Source of estrogen after menopause?

A

Peripheral conversion of androgens

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84
Q

Best test to confirm menopause?

A

↑↑ FSH

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85
Q

What does Menopause produce?

A

“HHAVOC”

Hirsutism, Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease

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86
Q

Menopause before age 40 indicates…

A

Premature ovarian failure

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87
Q

Menorrhagia

A

Heavy and/or prolonged menses

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88
Q

Average length of menses

A

3-5 days

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89
Q

Average blood loss during menses

A

35mL (10-80)

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90
Q

Metrorrhagia

A

Irregular menses

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91
Q

Dysmenorrhea

A

Painful menses

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92
Q

As women approach menopause, how does their cycle change

A

Follicular part becomes shorter. Failure of ovaries to produce follicles and estrogen –> ↑↑ FSH and earlier LH/FSH surge

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93
Q

Perimenopause
What is it?
How long does it last?

A

Irregular/skipped menses and beginning of vasomotor symptoms

Can last 5-10 years before menopause

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94
Q

Menopause definition

A

12 months of amenorrhea

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95
Q

Mechanisms of osteoporosis in menopause

A

Estrogen –/ bone resorption by osteoclasts

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96
Q

Leuprolide
Mechanism
Uses
Toxicity

A

GnRH analog
Pulsatile –> Agonist
Continuous –> Antagonist (downregulation of GnRH receptors in pituitary –> ↓ FSH/LH
Pulsatile: treats infertility
Continuous: Endometriosis, Prostate cancer (w/ Flutamide), Uterine fibroids, Precocious puberty
Tox: Antiandrogen, Nausea, Vomiting

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97
Q

Testosterone, Methyltestosterone
Mechanism
Use
Toxicity

A

Agonist for androgen receptors
Treats: hypogonadism, Promotes development of secondary sex characteristics, Stimulation of anabolism to promote recovery after burn injury
Tox: Masculinization in females, Reduces intratresticular testosterone in males by inhibiting release of LH which leads to gonadal atrophy, Premature closure of epiphyseal plate, ↑LDL, ↓HDL

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98
Q

Names of antiandrogens

A

Finasteride, Flutamide, Ketoconazole, Spironolactone

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99
Q 
Finasteride 
Kind of drug
MoA
Uses
Tox
A

Antiandrogen
–/ 5α Reductase which turns T into DHT
Treats BPH and hair loss
Breast growth

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100
Q

Flutamide
Kind of drug
MoA
Uses

A

Antiandrogen
Nonsteroidal competitive inhibitor of androgens at the testosterone receptor
Treats prostate carcinoma

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101
Q 
Ketoconazole
Kind of drug
MoA
Uses
Toxicity
A

Antiandrogen
Inhibits steroid synthesis (–/ 17,20 desmolase)
Treats PCOS to prevent hirsutism
Tox: gynecomastia and amenorrhea

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102
Q 
Spironolactone 
Kind of drug
MoA
Uses
Toxicity
A

Antiandrogen
Inhibits steroid binding
Treats PCOS to prevent hirsutism
Tox: gynecomastia and amenorrhea

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103
Q 
Estrogens 
Names
MoA
Use
Tox
Contraindication
A

Ethinly, Estradiol, DES, Mestranol
Binds Estrogen receptors
Treats Hypogonadism or Ovarian Failure, Menstrual abnormalities, HRT in postmenopausal women
Used in men to treat androgen dependent prostate cancer
Tox: ↑ risk of endometrial cancer, bleeding in postmenopausal women, clear cell carcinoma of the vagina/cervix in females exposed to DES in utero, ↑ risk of thrombi
ER+ breast cancer, history of DVTs

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104
Q

Names of Selective Estrogen Receptor Modulators (SERMs)

A

Clomiphene, Tamoxifen, Raloxifene

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105
Q 
Clomiphene 
Kind of Drug
MoA
Uses
Toxicity
A

SERM
Partial agonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and ↑ LH and FSH from pituitary.
Treats infertility and PCOS
Tox: Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances

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106
Q

Tamoxifen
Kind of Drug
MoA
Uses

A

SERM
Antagonist of estrogen receptors in breast tissue
Treats and prevents recurrence of ER+ breast cancer

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107
Q

Raloxifene
Kind of Drug
MoA
Uses

A

SERM
Agonist of estrogen receptors in bone and reduces bone resorption
Treats osteoporosis

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108
Q

Hormone Replacement Therapy
Uses
Toxicity

A

Used for the relief or prevention of menopausal symptoms (hot flashes, vaginal atrophy, etc) and osteoporosis (by ↑ estrogen –> ↓ osteoclast activity)
Unopposed use of estrogen –> ↑ risk of endometrial cancer, so progesterone is added. Possible ↑ CV risk

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109
Q

Anastrozole/Exemestane
MoA
Uses

A

Aromatase inhibitor used to treat postmenopausal women with breast cancer

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110
Q

Progestins
MoA
Uses

A

Binds progesterone receptors. Reduces growth and ↑ vascularization of endometrium
Used in oral contraceptives and treatment of endometrial cancer and abnormal uterine bleeding

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111
Q 
Mifepristone (RU-486)
MoA
Co-administered with...
Use
Tox
A

Competitive inhibitor of progestins at progesterone receptor
Termination of pregnancy. Administered w/ misoprostol (PGE)
Tox: Heavy bleeding, GI effects (nausea, vomiting, anorexia), Abdominal pain

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112
Q

Oral Contraception
What does it consist of?
MoA
Contraindications

A

Progestins + Estrogen
E and P –/ LH/FSH which leads to prevention of estrogen surge. No estrogen surge –> no LH surge. No LH surge –> no ovulation
Progestins cause thickening of the cervical mucus, thereby limiting access of sperm to uterus.
Progestins –/ endometrial proliferation making it less suitable for implantation
Contraindicated in smokers >35 (CV events), Hx of Thromboembolism and stroke or Hx of estrogen dependent tumors

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113
Q

Terbutaline
MoA
Uses

A

β2 agonist that relaxes uterus

Reduces premature uterine contractions

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114
Q

Tamsulosin
MoA
Uses
Selectivity

A

α1 antagonist used to treat BPH by inhibiting smooth muscle contraction
Selective for α1A and α1D (on prostate) vs α1B (vasculature)

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115
Q 
Sildenafil, Vardenafil
MoA
Uses
Tox
Contraindications
A

–/ Phosphodiesterase 5 causing an ↑ in cGMP, smooth muscle relaxation in corpus cavernosum, ↑ blood flow, and penile erection
Treats erectile dysfunction
Tox: “Hot and sweaty, but then Headache , Heartburn, Hypotension”
Headache, flushing, dyspnea, impaired blue-green color vision, Hypotension
Risk of life threatening hypotension in nitrate users

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116
Q

Danazol
MoA
Uses
Tox

A

Synthetic androgen that is a partial agonist at androgen receptor
Endometriosis and hereditary angioedema
Wt Gain, Edema, Acne, Hirsutism, Masculinization, ↓HDL, Hepatotoxicity

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117
Q 
Endometriosis 
What is it?
What tissue is affected?
What does it cause?
What causes it?
A 
Non-neoplastic endometrial glands/stroma in abnormal locations
In Ovary or on Peritoneum  
Cyclic bleeding (menstrual type) resulting in blood filled "chocolate cysts"
Caused by retrograde menstrual flow
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118
Q

Endometriosis
Clinical manifestation?
Treatment

A

Dysmenorrhea, Menorrhagia, Dyspareunia, Infertility
Uterus is normal size
Treat with oral contraceptives, NSAIDs, Leuprolide, Danazol

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119
Q

Adenomyosis
What is it?
Clinical manifestation
Treatment

A

Endometrium within myometrium
Menorrhagia, Dysmenorrhea, Pelvic pain
Enlarged uterus
Hysterectomy

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120
Q 
Cervical Dysplasia and Carcinoma In Situ
Description 
Where does it begin and extend?
Classification 
Histology
A

Disordered epithelial growth
Begins at basal layer of squamo-columnar junction and extends outwards
CIN1, CIN2, CIN3 (severe dysplasia or carcinoma in situ) depending on how high the basal cells extend
Koilocytes: raisinoid nuclei with perinuclear halo

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121
Q 
Cervical Dysplasia and Carcinoma In Situ
Viral cause?
Mechanism of viral cause?
Prevention?
Risk if untreated 
Risk factors
A

HPV16 and HPV18 (E6 –/ p53 andE7 –/ RB)
Vaccine available
May progress to invasive carcinoma if left untreated
Multiple sexual partners, smoking , early intercourse, HIV

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122
Q

Cervical Invasive Carcinoma
Most often what kind of carcinoma?
Screen?
Complications

A

Often squamous cell carcinoma
Pap smear
Lateral invasion can block ureter leading to renal failure

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123
Q 
PCOS
PathoPhys
Gross
Clinical manifestation 
Associated w/
Increased risk for
A

↑ frequency of pulsatile GnRA release –> ↑LH + ↓FSH –> anovulation –> no progesterone
Hyperandrogenism b/c of deranged steroid synthesis by Theca cells
Bilaterally enlarged, cystic ovaries
Amenorrhea, infertility, obesity, hirsutism
Associated with insulin resistance
Risk for endometrial cancer (↑ estrogen + no progesterone to oppose –> ↑ aromatization of testosterone in fat)

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124
Q

PCOS treatment

A

Wt reduction
Low does Oral Contraceptive or medroxyprogesterone (↓ LH and androgenesis)
Spironolactone (acne and hirsutism)
Clomiphene (infertility)
Meformin (diabetes or metabolic syndrome)

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125
Q 
Endometrial hyperplasia 
What is it?
What causes it?
Increased risk for...
Presentation 
Risk factors
A 
Abnormal endometrial gland proliferation
Caused by excess estrogen stimulation
↑ risk for endometrial carcinoma 
Postmenopausal vaginal bleeding
Anovulatory cycle, HRT, PCOS, Granulosa Cell Tumor
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126
Q 
Endometrial Carcinoma 
Frequency 
Epidemiology 
Presentation
Typically preceded by
Risk factors 
Prognosis
A

Most common gynecologic malignancy
Peak occurrence at 55-65
Vaginal bleeding
Typically preceded by endometrial hyperplasia
Prolonged use of estrogen w/o progesterone, obesity, diabetes, HTN, nulliparity, late menopause
↑ myometrial invasion –> poor prognosis

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127
Q

Types of Myometrial tumors

A

Leiomyoma (fibroid)

Leiomyosarcoma

128
Q 
Leiomyoma
Type of tumor
Frequency
Gross
Epidemiology
What kind of tissue
Malignant?
A

Myometrial tumor
Most common of all tumors in females
Multiple tumors with well-demarcated borders
↑ incidence in blacks. Peak at 20-40
Benign smooth muscle tumor
Malignant transformation to Leiomyosarcoma is rare

129
Q 
Leiomyoma
Hormone sensitive?
Presentation
Complications 
Histology
A

Estrogen sensitive: tumor size ↑ w/ pregnancy and ↓ w/ menopause
May be asymptomatic, cause abnormal uterine bleeding, miscarriage
Severe bleeding may lead to Iron Deficiency Anemia
Whorled pattern of smooth muscle fibers

130
Q 
Leiomyosarcoma
Kind of tumor
Gross
Where does it arise from?
Epidemiology
Prognosis
A 
Myometrial tumors
Bulky, irregular shaped tumor with areas of necrosis and hemorrhage. May protrude from cervix and bleed
Typically arising de novo
↑ incidence in middle aged black women
Highly aggressive w/ tendency to recur
131
Q 
Hydatidiform Moles
What are they?
Types
Presentation
Precursor of...
Serum marker 
Gross
Potential complication 
Treatment
A 
Cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast) 
Complete vs Partial
Presents with abnormal vaginal bleeding
Most common precursor of choriocarcinoma
↑βhCG
Honeycomb uterus or cluster of grapes appearance. Enlarged uterus
Uterine rupture 
dilation and curettage and methotrexate
132
Q 
Complete Hydatidiform moles
Appearance 
Fetus?
Karyotype
hCG
Uterine size
Conversion to choriocarcinoma 
Fetal parts
Components 
Risk of complications
A 
Snowstorm appearance with no fetus during 1st sonogram
46XX, 46XY
↑↑↑↑ hCG
↑ uterine size
2% choriocarcinoma
No fetal parts
2 sperm (from same sperm that replicated) + empty egg
15-20% malignant trophoblastic disease
133
Q 
Partial Hydatidiform moles
Karyotype
hCG
Uterine size
Conversion to choriocarcinoma 
Fetal parts
Components 
Risk of complications
A 
69XXX, 69XXY, 69XYY
↑ hCG
No change in uterine size
Rare choriocarcinoma 
Has fetal parts
2 sperm + 1 egg
Low risk of malignancy
134
Q

Classical Preeclampsia presentation

A

Pregnant women with HTN, Proteinuria, and Edema

135
Q

Classical Presentation of Eclampsia

A

Preeclampsia + Seizures

136
Q 
Preeclampsia
Frequency
When
↑ risk in...
Caused by
Associated w/
Mortality results from
A

7% of pregnant women from 20 weeks to 6 weeks postpartum
↑ risk in pts w/ HTN, Diabetes, Chronic Renal Disease, Autoimmune disorders
Impaired vasodilation of spiral arteries –> Placental ischemia –> ↑ vascular tone
Associated with HELLP syndrome
Death from cerebral hemorrhage and ARDS

137
Q

HELLP Syndrome

A

Hemolysis, Elevated Liver enzymes, Low Platelets

138
Q

Clinical Manifestations of Preeclampsia

Lab findings

A

Headache, Blurred vision, Abdominal pain, Edema of face and extremities, altered mentation, hyperreflexia
Thrombocytopenia and Hyperuricemia

139
Q

Treatment Preeclampsia

A

Delivery of fetus as soon as possible, Bed rest, monitoring, treat HTN
IV MgSulfate to prevent seizures

140
Q

Ovarian germ cell tumors most common in…

A

Adolescents

141
Q 
Dysgerminoma 
What kind of tumor?
Malignant?
Equivalent in male?
Histology
Associated w/
Markers
A 
Ovarian germ cell tumor
Malignant
Equivalent to male seminoma but rarer (1% over 30%)
Sheets of uniform cells
Associated with Turners Syndrome 
hCG and LDH
142
Q 
Choriocarcinoma in females 
What kind of tumor?
Frequency
Malignant 
Who develops it?
When does it develop?
Source
Histology
What other pathologies is it related to?
Metastases
Serum markers
A

Ovarian germ cell tumor
Rare but malignant
Develops during or after pregnancy in mother or baby
From trophoblastic tissue
No chorionic villi and ↑ theca-lutein cysts
On spectrum with moles as gestational trophoblastic neoplasms
Early homogenous spread to lungs
hCG

143
Q 
Yolk Sac (Endodermal Sinus) Tumor in women 
What kind of tumor?
Malignant?
Location
What kind of pt?
Gross
Histology 
Marker
A

Ovarian germ cell tumor
Aggressive malignancy in ovaries/testes and sacrococcygeal area of young children
Yellow, friable, solid masses
50% of Schiller-Duval bodies (resemble glomeruli)
AFP

144
Q 
Teratoma in women 
What kind of tumor
Frequency 
Types of tissue?
Types
A

Ovarian germ cell tumor
90% of ovarian germ cell tumors
Contains cells from 2 or 3 germ layers
Mature vs. Immature

145
Q

Mature Teratoma in women
Gross
Frequency
Malignant?

A

Dermoid Cyst
Most common ovarian germ cell tumor
Mostly benign

146
Q

Immature Teratoma in women
Malignant?
Gross
Presentation

A

Aggressively malignant
Can have Struma Ovarii (functional thyroid tissue)
Can present as hyperthyroidism

147
Q 
Serous Cystadenoma 
Kind of tumor
Frequency
Distribution 
Histology
Malignant?
A 
Ovarian non-germ cell tumor
45% of ovarian tumors
Bilateral
Lined with fallopian tube-like epithelium 
Benign
148
Q

Marker for Ovarian cancer?

A

↑ CA-125

Good for monitoring progression but not screening

149
Q 
Serous cystadenocarcinoma 
Kind of tumor
Frequency
Distribution 
Histology
Malignant?
Genetic risk factors
A 
Ovarian non-germ cell tumor
45% of ovarian tumors
Bilateral 
Psammoma bodies 
Malignant 
BRCA1, BRCA2, HNPCC
150
Q

Mucinous Cystadenoma
Kind of tumor
Malignant
Histology

A

Ovarian non-germ cell tumor
Benign
Multilocular cyst lined by mucus secreting epithelium. Intestine-like tissue

151
Q

Mucinous Cystadenocarcinoma
Kind of tumor
Malignant?
Complication

A

Ovarian non-germ cell tumor
Malignant
Pseudomyxoma peritonei - intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor

152
Q 
Brenner Tumor
Kind of tumor
Malignant
Distribution
Gross
Histology
A 
Ovarian non-germ cell tumor
Benign
Unilateral
Looks like Bladder. Solid tumor that is pale yellow-tan color and appears encapsulated 
Coffee bean nuclei on H&amp;E
153
Q 
Fibromas
Kind of tumor?
Histology
Complication 
Clinical Manifestation
A

Ovarian non-germ cell tumor
Bundles of spindle shaped fibroblasts
Meigs’ Syndrome
Pulling sensation in groin

154
Q

Meigs Syndrome

A

Ovarian fibroma + ascites + hydrothorax

155
Q 
Granulosa Cell Tumor
What kind of tumor
Hormones 
Complications in kids vs adults
Histology 
Presentation
A

Ovarian non-germ cell tumor
Secretes estrogen
Precocious puberty in children
endometrial hyperplasia or carcinoma in adults
Call-Exner bodies (small follicles filled with eosinophilic secretions)
Abnormal uterine bleeding

156
Q

Krukenberg Tumors
Kind of tumor
Source
Histology

A

Ovarian non-germ cell tumor
GI malignancy that metastasizes to ovaries
Mucin secreting signet cell adenocarcinoma

157
Q

Squamous Cell Carcinoma of the Vagina Usually secondary to…

A

SCC of cervix

158
Q

Women at risk for Clear Cell Adenocarcinoma of the Vagina

A

DES exposure in utero

159
Q

Sarcoma Botryoides (rhabdomyosarcoma variant)
Kind of tumor
Classic pt
Histology

A

Vaginal Tumor
Girls <4
Spindle shaped, Desmin+ tumor cells

160
Q 
Dizygotic twins
Frequency
Egg #
Amniotic sacs
Placentas
A

80% of twins
2 eggs
2 separate amniotic sacs
2 separate placentas (chorions)

161
Q 
Monozygotic twins that split day 0-4
Stage
Frequency 
Placenta
Amniotic sacs 
Chorion
A 
Morula
25%
Fused or separate placenta 
Diamniotic
Dichorionic
162
Q 
Monozygotic twins that split day 4-8
Stage
Frequency 
Amniotic sacs 
Chorion
A

Blastocyst
75%
Diamniotic
Monochorionic

163
Q

Monozygotic twins that split day 8-12
Frequency
Amniotic sacs
Chorion

A

Less than 1%
Monoamniotic
Monochorionic

164
Q

Monozygotic twins that split after day 13

A

Monoamniotic
Monochorionic
Conjoined

165
Q

Fetal Components of the placenta

A

Cytotrophoblast and Syncytiotrophoblast

166
Q

Cytotrophoblast
Where is it?
What is it made from?
Where is it from?

A

Inner layer of chorionic villi
Cytotrophoblast made from Cells
Fetal component

167
Q

Syncytiotrophoblast
Where is it?
What does it secrete?

A

Outer layer of chorionic villi

Secretes hCG

168
Q

Maternal component of placenta
Name
Derived from?

A

Decidua Basalis

Derived from endometrium

169
Q

Where is maternal blood in the placenta?

A

In Lacunae

170
Q

What makes up the Umbilical Cord?

A

2 Umbilical arteries and 1 Umbilical vein

171
Q

Function of umbilical arteries

Source?

A

Return deoxygenated blood from fetal internal iliac arteries to placenta

172
Q

Function of umbilical vein?

What does it drain into?

A

Supplies oxygenated blood from placenta to fetus

Drains via ductus venosus into IVC

173
Q

Single umbilical artery is associated with…

A

Congenital and Chromosomal Anomalies

174
Q

What are the umbilical arteries and veins are derived from?

A

The Allantois

175
Q

Urachal Duct
What is it?
Development?
Failure to obliterate?

A

A duct between bladder and yolk sac
3rd week: Yolk sac forms allantois which extends into urogenital sinus. Allantois becomes urachus
Patent Urachus: urine discharge from the umbilicus
Vesicourachal diverticulum: outpouching of bladder

176
Q 
Vitelline duct 
Name
Function
When is it obliterated 
Failure to obliterate
A

Omphalo-Mesenteric Duct
Connects yolk sac to midgut lumen
Obliterated at week 7
Vitelline fistula: meconium discharge from umbilicus
Meckel’s Diverticulum: Ectopic gastric and pancreatic tissue –> melena, periumbilical pain, ulcer

177
Q

1st Aortic Arch forms

A

Maxillary artery (branch of external carotid)

178
Q

2nd Aortic Arch forms

A

Stapedial artery and Hyoid artery

179
Q

3rd Aortic Arch forms

A

Common Carotid artery and proximal part of Internal Carotid artery

180
Q

4th Aortic Arch forms

A

L: Aortic arch
R: Proximal part of Subclavian artery

181
Q

6th Aortic Arch forms

A

Proximal part of pulmonary arteries and (on left only) ductus arteriosus

182
Q

Branchial Apparatus
AKA
Composition with origin

A 
Pharyngeal Apparatus
"CAP" 
Clefts (grooves) from Ectoderm 
Arches from Mesoderm (muscles, arteries) and neural crest cells (bones, cartilage)
Pouches from Endoderm
183
Q

Branchial Clefts develop into

A

1st: External auditory meatus

2nd - 4th: form temporary cervical sinus which are obliterated by proliferation of 2nd arch mesenchyme

184
Q

Persistent Cervical Sinus

A

Branchial cleft cyst within lateral neck

185
Q 
1st Branchial Arch 
Cartilage
Muscles 
Nerves 
Pathology
A

Meckel’s cartilage: Mandible, Malleus, incus, spheno-Mandibular ligament
Muscles of Mastication (Temporalis, Masseter, Lat and Med Pterygoids), Mylohyoid, Anterior belly of the digastric, Tensor Tympani, Tensor Veli Palatini
V2 and V3
Treacher Collins Syndrome –> 1st arch crest fails to migrate –> Mandibular hypoplasia and facial abnormalities

186
Q

2nd Branchial Arch
Cartilage
Muscles
Nerves

A

Reichert’s Cartilage (Stapes, Styloid Process, Lesser horn of the Hyoid, Stylohyoid ligament)
Muscles of facial expression, Stapedius, Stylohyoid, Posterior Belly of the Digastric
CNVII

187
Q 
3rd Branchial Arch 
Cartilage
Muscles 
Nerves 
Pathology
A

Greater horn of hyoid
Stylopharyngeus
CN IX (“swallow stylishly”)
Congenital Pharyngo-Cutaneous Fistula: Persistence of cleft and pouch –> Fistula between tonsillar area, cleft in lateral neck

188
Q

4th - 6th Branchial Arch
Cartilage
Muscles
Nerves

A

Thyroid, Cricoid, Arytenoids, Corniculate, Cuneiform
4th: Most Pharyngeal Constrictors; Cricothyroid, Levator Veli Palatini
6th: All intrinsic muscles of larynx except cricothyroid
CNX: 4th is superior laryngeal branch (“simply swallow”), 6th is recurrent laryngeal branch (“speak”)

189
Q

Branchial Arches Mnemonic

A

Chew, Smile, Swallow Stylishly, Simply Swallow, Speak

190
Q

What forms posterior 1/3 of tongue

A

Branchia Arches 3 and 4

191
Q

What does Branchia Arch 5 become?

A

5 makes no major developmental contributions

192
Q

1st Branchial Pouch
Develops into
What does it contribute to?

A

Middle Ear Cavity, Eustachian Tube, Mastoid Air Cells

Contributes to Endoderm-lined structures of ear

193
Q

2nd Branchial Pouch develops into…

A

Epithelial lining of palatine tonsil

194
Q

3rd Branchial pouch
Develops into…
Where does it end up

A

Dorsal wings develop into inferior parathyroids
Ventral wing develops into Thymus
Ends up below 4th

195
Q

4th Branchial pouch develops into…

A

Dorsal wings develop into superior parathyroids

196
Q

DiGeorge Syndrome
What develops abnormally
PathoPhys

A

Aberrant development of 3rd and 4th Branchial pouches

T cell deficiency (Thymic aplasia) and Hypocalcemia (parathyroid doesn’t develop)

197
Q

Cleft Lip

A

Failure of fusion of maxillary and Medial Nasal Processes (formation of primary palate)

198
Q

Cleft Palate

A

Failure of fusion of the lateral palatine processes, the nasal septum, and/or the median palatine process (formation of secondary palate)

199
Q

Cleft Lip vs Cleft Palate

A

2 distinct etiologies but often occur together

200
Q

Female genital development
What kind of pathway?
Ducts?

A

Default pathway

Mesonephric duct degenerates and Paramesonephric duct develops

201
Q

Phys of male genital development

A

SRY produces testes determining factor
Sertoli cells secrete Mullerian Inhibitory Factor.
Leydig cells secrete Testosterone that stimulate development of mesonephric ducts

202
Q

Paramesonephric duct
Name
What does it develop into?
Presentation of defect?

A

Mullerian Duct
Fallopian tubes, uterus, upper vagina
Primary amenorrhea with fully developed secondary sex characteristics

203
Q

Mesonephric Duct
Name
What does it develop into?

A

Wolffian duct
“SEED”
Develops into Seminal vesicles, Epididymis, Ejaculatory duct, Ductus deferens

204
Q

Bicornuate Uterus
What is it?
What can it lead to?

A

Incomplete fusion of Mullerian duct

Can lead to urinary tract abnormalities and miscarriages

205
Q

What does DHT do?

A

Promotes development of male external genitalia and prostate

206
Q

What happens if there are no sertoli cells or no MIF?

A

Development of both male and female internal genitalia and male external genitalia

207
Q 
5αReductase Deficiency 
Chromosomes, Genitalia, Inheritance 
PathoPhys 
Presentation 
Hormonal findings
A

XY
Internal genitalia normal
AR
Inability to convert T to DHT
Ambiguous genitalia until puberty, when T causes masculinization and ↑ growth of external genitalia
T and Estrogen levels are normal. LH normal or ↑

208
Q

Genital Tubercle
Male
Female

A

Male: Glans, Corpus Cavernosum, Spongiosum
Female: Glans Clitoris, Vestibular Bulbs

209
Q

Urogenital Sinus
Male
Female

A

Bulbourethral glands, Prostate

Greater vestibular glands of Bartholin and Urethral and Paraurethral glands of Skene

210
Q

Urogenital folds
Male
Female

A

Ventral shaft of penis (penile urethra)

Labia Minora

211
Q

Labioscrotal swelling
Male
Female

A

Scrotum

Labia Majora

212
Q 
Hypospadias 
What is it?
What causes it?
Frequency
Why treat it?
A

“Hypo is Below”
Abnormal opening of penile urethra on inferior (ventral) side of penis
Due to failure of urethral folds to close
More common than epispadias
Fix to prevent UTIs

213
Q

Epispadias
What is it?
What causes it?
Association

A

“When you have Epispadias you hit your Eye when you pEE”
Abnormal opening of penile urethra on superior (dorsal) side of penis
Due to faulty positioning of genital tubercle
Extrophy of the bladder

214
Q

Gubernaculum
What is it?
Male remnant
Female remnant

A

Band of Fibrous Tissue
Anchors Testes within scrotum
Ovarian ligament and Round ligament of the uterus

215
Q

Processus Vaginalis
What is it?
Male remnant
Female remnant

A

Evagination of peritoneum
Forms tunica vaginalis
Obliterated

216
Q

Venous drainage of gonads?

A

L ovary/teste –> L gonadal vein –> L renal vein –> IVC

R ovary/teste –> R gonadal vein –> IVC

217
Q

Lymphatic drainage of ovaries/testes

A

Para-Aortic Lymph Nodes

218
Q

Lymphatic drainage of distal 1/3 of vagina, vulva, and scrotum

A

Superficial Inguinal Nodes

219
Q

Lymphatic drainage of Proximal 2/3 of vagina and uterus?

A

Obturator, External Iliac and Hypogastric Nodes

220
Q

On which side is Varicocele more common?

A

More common on Left because L venous pressure > R venous pressure because L spermatic vein enters L renal vein at 90 degrees, so flow is less continuous on Left

221
Q

Suspensory Ligament of the Ovaries
Connects
Structures contained

A

Ovaries to lateral pelvic wall

Ovarian vessels

222
Q

What can be damaged during oophorectomy?

A

Ureter is at risk during ligation of ovarian vessels in oophorectomy

223
Q

Cardinal Ligament
Connects
Structures contained

A

Cervix to side wall of pelvis

Uterine vessels

224
Q

What can be damaged during hysterectomy?

A

Ureter at risk of injury during ligation of uterine vessels

225
Q 
Round Ligament of the Uterus 
Connects 
Structures contained
Derivative from what?
What does it travel through?
A

Uterine Fundus to Labia Majora
Artery of Sampson
Derivative of Gubernaculum
Travels through round inguinal canal

226
Q

Broad Ligament
Connects
Structures contained
Components

A

Uterus, Fallopian Tubes, and Ovaries to Pelvic side wall
Ovaries, Fallopian tubes, Round ligaments of the uterus
Mesosalpinx, Mesometrium, Mesovarium

227
Q

Ligament of the ovary
Connects
Structures contained
Derivative from what?

A

“Latches ovary to Lateral uterus”
Medial pole of ovary to lateral uterus
None
Derivative of gubernaculum

228
Q

Vagina histology

A

Stratified Squamous Epithelium, Nonkeritinizing

229
Q

Ectocervix histology

A

Stratified Squamous

230
Q

Endocervix histology

A

Simple Columnar

231
Q

Uterus Histology

A

Simple columnar, Pseudostratified tubular glands

232
Q

Fallopian tube histology

A

Simple columnar, ciliated

233
Q

Ovary histology

A

Simple cuboidal

234
Q

Pathway of sperm

A 
"SEVEN UP"
Seminiferous tubules
Epididymis
Vas deferens
Ejaculatory duct
Nothing 
Urethra
Penis
235
Q

Erection
System responsible?
Nerve
Pathway

A

Parasympathetic nervous system
Pelvic nerve
NO –> ↑ cGMP –> smooth muscle relaxation –> vasodilation –> proerectile

236
Q

Nervous pathology of anti-erection

A

NE –> ↑ [Ca] –> smooth muscle contraction –> vasoconstriction –> antierectile

237
Q

Nervous system responsible for emission

Nerve?

A

Sympathetic nervous system

Hypogastric nerve

238
Q

Nerves responsible for Ejaculation

A

Visceral and Somatic Nerves

Pudendal nerve

239
Q

Spermatogonia
Function
What do they produce
Location

A

Maintain germ pool
Produce Primary Spermatocytes
Line seminiferous tubules

240
Q 
Sertoli cells 
What do they secrete?
Connections between cells?
Function 
Effects of Temp? What changes temp?
A

Secretes inhibin (inhibits FSH), Androgen binding protein (maintains local levels of testosterone), AMH
Tight junctions form blood-testis barrier –> isolate gametes from autoimmune attack
Support and nourish spermatozoa, Regulate spermatogenesis
Temp sensitive: Varicocele or Cryptorchidism –> ↑ Temp –> ↓ sperm production and ↓ inhibin

241
Q

Leydig Cells
Secrete
Effects of Temp?
Location

A

Secrete Testosterone
Unaffected by Temp
Interstitium

242
Q

Male Meiosis

A

Spermatogonium (2N2C) –> Primary Spermatocytes (2N4C)–> [Meiosis I] –> Secondary Spermatocyte (1N2C) –> [Meiosis II] –> Spermatid (NC) –> [Spermiogenesis] –> Mature spermatozoon

243
Q

Where are the tight junctions between Sertoli cells

A

Between Spermatogonium and Primary Spermatocytes

244
Q

Time for full development of sperm?

A

2 months

245
Q

Process of spermatogenesis

A

Loss of cytoplasmic contents and gain of acrosomal cap

246
Q

Hormone pathways of Testes

A

Hypothalamus –> GnRH –> AP –> FSH and LH
FSH –> Sertoli cells –> ABP and Inhibin
Inhibin –/ AP
LH –> Leydig cells –> Testosterone –/ Hypothalamus and AP

247
Q

Androgens
Names w/ potency
Source

A

DHT > Testosterone > Androstenedione

T and D from testes, AnDrostenedione from ADrenal gland

248
Q

Testosterone Functions

A

Differentiation of epididymis, vas deferens, seminal vesicles (internal genitalia except prostate)
Growth spurt (penis, seminal vesicles, sperm, muscles, RBCs)
Deepening of voice
Closing of epiphyseal plates (via estrogen converted to testosterone)
Libido

249
Q

DHT functions
Early
Late

A

Differentiation of penis, scrotum and prostate

Prostate growth, balding, sebaceous gland activity

250
Q

What converts testosterone and androstenedione into estrogen

A

Aromatase in adipose tissue

251
Q 
Klinefelter's Syndrome 
Chromosomes 
Pathways 
Presentation 
Histo
A

XXY
Dysgenesis of seminiferous tubule –> ↓ inhibin –> ↑ FSH
Abnormal Leydig cell function –> ↓ testosterone –> ↑ LH –> ↑ Estrogen
Testicular atrophy, eunuchoid body shape, Tall, Long extremities, Gynecomastia, female hair distribution, Developmental delay
Barr body

252
Q 
Turners Syndrome 
Chromosomes 
Pathways 
Presentation 
Gross anatomy 
Risk for?
Histo
A

XO
↓ estrogen –> ↑ LH and FSH
Short, shield chest, amenorrhea, menopause before menarche
Streak ovaries, bicuspid aortic valve, defective lymphatics –> webbing of neck (cystic hygroma), lymphedema in feet and hands, Preductal coarctation of the aorta, horseshoe kidney
Dysgerminoma
No barr body

253
Q

Double Y male
Presentation
Risks

A

Phenotypically normal, very tall, severe acne, normal fertility
Antisocial behavior and autism spectrum disorder

254
Q

Defective androgen receptor
Testosterone
LH

A

Testosterone ↑

LH ↑

255
Q

Testosterone secreting tumor or exogenous steroids
Testosterone
LH

A

Testosterone ↑

LH ↓

256
Q

Primary Hypogonadism
Testosterone
LH

A

Testosterone ↓

LH ↑

257
Q

Hypogonadotropic Hypogonadism
Testosterone
LH

A

Testosterone ↓

LH ↓

258
Q 
Female pseudohermaphrodite 
Chromosomes 
Gonads
External genitalia 
Cause
A

XX
Ovaries
Virilized or ambiguous genitalia
Exposure to androgens during early gestation: congenital adrenal hyperplasia or exogenous administration

259
Q 
Male pseudohermaphrodite
Chromosomes 
Gonads
External genitalia 
Cause
A

XY
Testes
Female or ambiguous
Androgen insensitivity syndrome is most common form

260
Q 
True Hermaphroditism 
Chromosomes 
Gonads 
Genitalia 
Frequency
A

XX or XXY
Ovotestis
Ambiguous genitalia
Very rare

261
Q 
Androgen Insensitivity Syndrome 
PathoPhys
External Genitalia
Internal Genitalia 
What do they develop?
Hormonal Findings?
A

Defective Androgen Receptor
Normal appearing female with female external genitalia but with scant genital hair
Rudimentary vagina. No Uterus or Fallopian tubes
Testes in Labia Majora that must be surgically removed
↑ Testosterone, Estrogen, and LH

262
Q

Kallmann Syndrome
PathoPhys
Presentation
Findings

A

Defective migration of GnRH cells and formation of olfactory bulb
Anosmia and lack of secondary sex characteristics
↓ GnRH, FSH, LH, T, and Sperm count

263
Q 
Abruptio Placentae 
What is it?
Associated with what?
↑ risk with...
Presentation 
Threat?
A 
Premature detachment of placenta 
DIC
Smoking, HTN, Cocaine 
Painful bleeding in 3rd trimester 
Life threatening for both fetus and mother
264
Q

Placenta Accreta
What is it?
↑ risk with…
Presentation

A

Defective decidual layer allows placenta to attach to myometrium –> No separation of placenta after birth
Prior C section, Inflammation, Placenta previa
Massive bleeding after delivery

265
Q

Placenta previa
What is it?
↑ risk with…
Presentation

A

Attachment of placenta to lower uterine segment over internal cervical os
Multiparity and prior C-section
Painless bleeding in any trimester

266
Q

Retained Placental Tissue leads to

A

Postpartum hemorrhage and ↑ risk of infection

267
Q 
Ectopic Pregnancy 
Most often location 
Presentation 
Dx
Risk factors 
Often confused with...
Histo
A

Fallopian tube
Amenorrhea, lower than expected ↑ in hCG, sudden abdominal pain w/ or w/o bleeding
US
Infertility, PID, Rupture appendix, Tubal surgery
Appendicitis
Endometrial biopsy shows decidualized endometrium but no chorionic villi

268
Q

Polyhydramnios
Amount
PathoPhys
Associated with…

A

More than 1.5L
Esophageal/Duodenal atresia –> inability to swallow amniotic fluid
Anencephaly

269
Q

Oligohydramnios
Amount
PathoPhys
What can it give rise to?

A

Less than .5L
Placental insufficiency, bilateral renal agenesis, or posterior urethral valves (in males) leading to inability to excrete urine
Potters Syndrome

270
Q

Endometritis
What is it?
Treatment

A

Inflammation of the endometrium with retained products of conception following delivery (vaginal, C-section, miscarriage, abortion, foreign body) leads to bacterial infection from vaginal or intestinal flora
Gentamycin + Clindamycin w/ or w/o Ampicillin

271
Q

Gynecologic tumor epidemiology
Incidence
Prognosis

A

Endometrial > Ovarian > Cervical

Ovarian > Cervical > Endometrial

272
Q

Premature Ovarian Failure
What is it?
Presentation
Findings

A

Premature atresia of ovarian follicles
Menopause before age 40
↓ estrogen, ↑ LH, ↑ FSH

273
Q

Most common causes of anovulation

A

Pregnancy, PCOS, Obesity, HPO axis abnormalities, Premature Ovarian Failure, Hyperprolactinemia, Thyroid disorders, Eating disorders, Cushing’s syndrome, Adrenal Insufficiency

274
Q

Follicular Cyst
What is it?
Associated with?
Frequency

A

Distention of unruptured graafian follicle
Hyperestrinism and Endometrial Hyperplasia
Most common ovarian mass in young women

275
Q

Corpus Luteum Cyst
What is it?
Course

A

Hemorrhage into persistent corpus luteum

Commonly regresses spontaneously

276
Q

Theca Lutein Cyst
#
Cause?
Associated with…

A

Bilateral and multiple
Gonadotropin stimulation
Choriocarcinoma and moles

277
Q

Hemorrhagic Cyst
What is it?
Course

A

Blood vessel rupture into cyst wall.
Cyst grows with ↑ blood retention
Usually self resolves

278
Q

Dermoid Cyst

A

Mature teratoma. Cystic growth with various tissues such as fat, hair, teeth, bone, cartilage

279
Q

Endometrioid Cyst
What is it?
How does it vary
Appearance with name

A

Endometriosis within ovary with cyst formation
Varies with menstrual cycle
When filled with dark, reddish brown blood it is called a chocolate cyst

280
Q

Course of milk flow in breast

A

Lobules –> Terminal duct –> Major duct –> Lactiferous sinus –> Nipple

281
Q 
Fibroadenoma of the breast 
Characteristics 
Epidemiology 
Malignant?
Hormones?
A

Small, Mobile, Firm Mass with sharp edges
Most common tumor in those under 35
↑ size and tenderness with ↑ estrogen
Not a precursor to breast cancer

282
Q 
Intraductal Papilloma 
Size 
Location 
Presentation 
Malignant
A

Small tumor
Lactiferous ducts, typically beneath areola
Serous or bloody nipple discarge
Benign with slight risk of carcinoma

283
Q 
Phyllodes Tumor 
Size
Type of tissue 
Appearance 
Epidemiology 
Malignancy
A 
Large and Bulky
Connective tissue and Cysts 
Leaf-like projections 
Most common in 6th decade of life 
Some may become malignant
284
Q 
Malignant Breast Tumors 
When does it present 
Location 
Markers 
Prognostic factors 
Risk factors
A

Common postmenopause
Terminal duct lobular unit in upper outer quadrant
Estrogen/Progesterone receptors or c-erbB2 (HER2 an EGF receptor)
Axillary lymph node involvement is important prognostic factor
↑ estrogen, total # of menstrual cycles, older age at 1st live birth, obesity, BRCA1, BRCA2 mutation

285
Q 
Ductal carcinoma in situ 
What kind of cancer?
What does it look like
Arise from
Malignancy?
A

Noninvasive malignant breast tumor
Fills ductal lumen
Arises from ductal hyperplasia
Early malignancy w/o basement membrane penetration

286
Q 
Comedocarcinoma 
What kind of cancer?
Type
Location 
Histo
A

Noninvasive malignant breast tumor
Subtype of DCIS
Ductal
Caseous Necrosis

287
Q 
Invasive Ductal Breast Cancer
What kind of cancer? 
Gross
Histo
Frequency 
Prognosis
A

Invasive malignant breast tumor
Firm, fibrous, “rock hard” mass with sharp margins
Small, glandular, duct-like cells with classic stellate morphology
Most common (76%)
Worst and most invasive

288
Q

Invasive Lobular Breast Cancer
What kind of cancer?
Distribution
Histo

A

Invasive malignant breast tumor
Bilateral with multiple lesions in the same location
Orderly row of cells (Indian File)

289
Q

Medullary Breast Cancer
What kind of cancer?
Histo
Prognosis

A

Invasive malignant breast tumor
Fleshy, Cellular, Lymphocytic infiltrate
Good prognosis

290
Q 
Inflammatory Breast Cancer 
What kind of cancer?
PathoPhys
Gross 
Prognosis
A

Invasive malignant breast tumor
Dermal lymphatic invasion by breast carcinoma blocking lymphatic drainage
Peau d’orange (breast skin resembles orange peel)
50% survival @ 5 years

291
Q 
Paget's Disease of Breast 
Gross 
Histo
What does it suggest?
Where else is it seen?
A

Eczematous patches on nipple
Paget cells = large cells in epidermis with clear halo
Suggets underlying DCIS
Also seen on vulva

292
Q

Fibrocystic Disease
Epidemiology
Presentation
What does it indicate

A

Most common cause of breast lumps from 25 to menopause
Premenstrual breast pain and multiple bilateral lesions. Fluctuations in size of mass
Does not indicate risk of carcinoma

293
Q

Fibrocystic Disease Subtypes

A

Fibrosis: hyperplasia of breast stroma
Cystic: Fluid filled, blue dome. Ductal dilation
Sclerosing adenosis: ↑ acini and intralobular fibrosis. Calcification. Often confused with cancer
Epithelial hyperplasia: ↑ # of epithelial cell layers in terminal duct lobule. ↑ risk of carcinoma with atypical cells. Occurs in women over 30

294
Q

Acute Mastitis
What is it?
When does it present
What are they at risk for?

A

Breast abscess
During breast feeding
Risk of bacterial infection through cracks in nipple by S aureus

295
Q

Fat Necrosis of the breast
Dangerous?
Presentation
What causes it?

A

Benign
Painless lump
Injury (usually unreported)

296
Q

What causes Gynecomastia?

A

Hyperestrogenism (Cirrhosis, Testicular tumor, Puberty, Old age)
Klinefelter’s Syndrome
Drugs (Estrogen, Marijuana, Heroic, Psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol, Ketoconazole)
“Some Drugs Create Awkward Knockers”

297
Q

Prostatitis
Presentation
Acute Cause
Chronic Cause

A

Dysuria, Frequency, Urgency, Low back pain
Acute: bacterial (E coli)
Chronic: bacterial or abacterial (most common)

298
Q

Benign Prostatic Hyperplasia
Epidemiology
PathoPhys
Malignant

A

Men over 50
Nodular enlargement of periurethral (lateral and middle) lobes compresses urethra
Not premalignant

299
Q 
Benign Prostatic Hyperplasia 
Presentation 
Complications 
Findings 
Treatment
A

Frequency, Nocturia, Dysuria, Difficulty starting and stopping stream
Distention and Hypertrophy of the bladder, Hydronephrosis, UTIs
↑ PSA
α1 antagonists (Terazosin, Tamsulosin), Finasteride

300
Q 
Prostatic Adenocarcinoma 
Epidemiology  
Location
Diagnosis 
Tumor markers 
Metastasis?
A 
Men over 50
Posterior lobe in peripheral zone 
↑ PSA and subsequent biopsy 
Prostatic Acid Phosphatase and PSA
Osteoblastic mets to bone present as lower back pain and ↑ AlkPhos
301
Q 
Cryptorchidism 
What is it?
Consequences 
Associated with what?
What increases risk for it?
Labs
A

Undescended testis
Impaired spermatogenesis (b/c of temp) but normal testosterone
Risk of germ cell tumor
Prematurity
↑ FSH, LH and ↓ inhibin (and testosterone if bilateral)

302
Q 
Varicocele 
PathoPhys
Consequences 
Location 
Can lead to...
Gross
How is Diagnosis made?
Treatment
A

Dilated veins in Pampiniform plexus b/c of ↑ venous pressure
Most common cause of scrotal enlargement
More common on Left
Infertility
Bag of Worms appearance
Diagnosed by US
Varicocelectomy, Embolization

303
Q 
Testicular Germ Cell Tumor 
Frequency 
Danger?
Can present as...
DDx
A

95% of all testicular tumors
Most often malignant
Can present as mixed germ cell tumor
Testicular mass that does not transilluminate

304
Q 
Seminoma 
What kind of cancer?
Malignant?
Presentation 
Epidemiology 
Histo 
Labs 
Treatment 
Prognosis
A

Testicular Germ Cell Tumor
Malignant
Painless homogenous testicular enlargement
Most common testicular tumor mostly affecting males 15-35
Large cells in lobules with watery cytoplasm and fried egg appearance
Placental ALP
Radiosensitive
Late metastasis with excellent prognosis

305
Q 
Yolk Sac (endodermal sinus) tumor in males 
What kind of cancer?
Gross
Analog
Histo
Labs
A 
Testicular Germ Cell Tumor 
Yellow, Mucinous 
Analogous to ovarian yolk sac tumor 
Schiller-Duval Bodies resemble primitive glomeruli 
↑ AFP
306
Q 
Choriocarcinoma in males 
What kind of cancer?
Danger?
Labs
What is it made of?
Metastasis?
Complications
A 
Testicular Germ Cell Tumor 
Malignant 
Increased hCG
Syncuytiotrophoblastic and Cytotrophoblastic elements 
Hematogenous mets to lungs 
Gynecomastia because of hCG
307
Q

Teratoma in male
What kind of cancer?
Malignant?
Labs

A

Testicular Germ Cell Tumor
Unlike in females, malignant in adults
Benign in children
↑ hCG +/or AFP in 50% of cases

308
Q 
Embryonal Carcinoma 
What kind of cancer?
Danger?
Presentation 
Prognosis 
Histo
Pure?
Labs
A

Testicular Germ Cell Tumor
Malignant
Painful
Worse prognosis that seminoma
Glandular/Papillary morphology
Pure version is rare, most commonly mixed
↑ hCG and normal AFP (if pure). ↑ AFP when mixed

309
Q

Testicular Non-Germ Cell Tumor
Frequency
Danger

A

5% of all testicular cancers

Mostly benign

310
Q 
Leydig cell cancer 
What kind of cancer 
Histo
What does it produce?
Presentation 
Gross
A 
Testicular non-Germ Cell Tumor
Reinke Crystals 
Androgen producing 
Gynecomastia in men, precocious puberty in boys 
Golden Brown color
311
Q

Sertoli cell Cancer
What kind of cancer
Description
Origin

A

Testicular non-Germ Cell Tumor
Androblastoma
From sex cord stroma

312
Q 
Testicular Lymphoma 
What kind of cancer?
Epidemiology 
Origin
Course
A

Testicular non-Germ Cell Tumor
Most common testicular caner in older men
Arises from lymphoma metastases to testes
Aggressive

313
Q

Tunica Vaginalis Lesions
What is it?
Presentation
Types w/ causes

A

Lesions in the serous covering of testis
Present as testicular masses that can be transilluminated (vs testicular tumors)
Hydrocele: ↑ fluid secondary to incomplete fusion of processus vaginalis
Spermatocele: Dilated Epididymal Duct

314
Q

Squamous Cell Carcinoma of the Penis
Epidemiology
Association

A

Asia, Africa, and South America

HPV and lack of circumcision

315
Q

Peyronie’s Disease

A

Bent Penis due to acquired fibrous tissue formation

316
Q

Priapism
What is it?
Causes

A

Painful sustained erection not associated with stimulation or desire
Trauma, Sickle Cell Disease (RBCs trapped in vascular channel), Medication (anticoagulants, PDE5 inhibitors, antidepressants, α blockers, cocaine

USMLE STEP 1 (25 decks)

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