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Embryo/Repro Flashcards

1
Q

What is seen with a mutation in the Sonic Hedgehog gene?

A

Holoprosencephaly

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2
Q

What is the function of the Wnt-7 gene?

A

Ventral-dorsal axis organization

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3
Q

What is the function of the FGF gene?

A

Found at apical ectodermal ridge (tip of limb). Stimulates mitosis of underlying mesoderm –> lengthening of limbs

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4
Q

What is the seen with mutation of the Homeobox genes?

A

Hox genes orient the embryo in the cranial-caudal direction. Mutations cause limbs in the wrong places.

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5
Q

When is a fetus most susceptible to teratogens?

A

Weeks 3-8

This is the embryonic period & is when most organs are formed.

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6
Q

When does gastrulation occur?

A

3 layers = Week 3 (trilaminar)

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7
Q

When during embryogenesis are the limbs formed?

A

4 limbs = Week 4

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8
Q

When can the sex of a baby be determined by US?

A

Week 10

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9
Q

When does the neural tube form during embryogenesis?

A

Weeks 3-4

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10
Q

What structures are formed from the neural crest?

A 
PNS neurons
Schwann cells
Melanocytes
Parafollicular thyroid cells
Pia & arachnoid
Bones of the skull
Aorticopulmonary septum
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11
Q

What are the mesodermal defects?

A

CV LATER:

Cardiac defects
Vertebral defects
Limb defects
Anal atresia
Tracheo-Esophageal fistula
Renal defects
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12
Q

What structures are formed from the endoderm?

A 
Lungs
Gut tube epithelium
Liver
Gallbladder
Pancreas
Thymus
Thyroid follicular cells
Parathyroid
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13
Q

What is the difference between agenesis & aplasia?

A

Agenesis = absent primordial tissue

Aplasia = Primordial tissue was present but organ is absent

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14
Q

What is the difference between Deformation & Malformation?

A

Malformation = intrinsic & occurred during embryogenesis

Deformation = Extrinsic & occurred after embryogenesis

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15
Q

What is the embryologic effect of ACE inhibitors?

A

Renal damage

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16
Q

What is the embryologic effect of alkylating agents?

A

Absence of digits & other anomalies

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17
Q

What is the embryologic effect of aminoglycosides?

A

CNVIII toxicity

Just like how they are ototoxic in adults

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18
Q

What is the embryologic effect of Lithium?

A

Ebstein’s anomaly

Ebstein’s = Atrialized RV = most of the right heart is atrium

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19
Q

What is the embryologic effect of phenytoin?

A

Fetal hydantoin syndrome:

Microcephaly
Dysmorphic craniofacial features
Hypoplastic distal phalanges & nails
Mental retardation
Cardiac defects
Intrauterine growth restriction
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20
Q

What is the embryologic effect of Tetracyclines?

A

Discolored teeth

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21
Q

What is the embryologic effect of thalidomide?

A

“Flipper” limb defects

ThaLIMBdomide

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22
Q

What is the embryologic effect of Valproic acid?

A

Inhibits maternal folate absorption –> neural tube defects

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23
Q

What is the embryologic effect of warfarin?

A

Bone deformities
Fetal hemorrhage
Ocular abnormalities

Use heparin during pregnancy

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24
Q

What is seen with cocaine use during pregnancy?

A

Abruptio placentae
Abnormal fetal development
Fetal addiction

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25
Q

What is seen with smoking during pregnancy?

A

Premature delivery
IUGR
ADHD

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26
Q

What can be seen in infants born to diabetic mothers?

A

Caudal regression syndrome (aka sacral agenesis; ranges from anal atresia to full blown sirenomelia)
Congenital heart defects
Neural tube defects
NRDS

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27
Q

When must separation occur to cause the various types of monozygotic twins?

A

dichorionic, diamniotic
4-8 days (morula) –> Monochorionic diamniotic
8-12 days (blastocyst) –> Mono-mono
> 13 days –> mono-mono & conjoined

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28
Q

What are the chorionic villi composed of?

Which cell type secretes hCG?

A

Cytotrophoblasts (inner layer)

Sincytiotrophoblasts (outer layer) - secrete hCG

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29
Q

What is the urachus?

What pathology is seen with it?

A

Allantois –> Urachus –> Median umbilical fold
Urachus is a duct between the bladder & yolk sack

1) Patent urachus –> Urine discharge from umbilicus
2) Vesiurachal diverticulum –> outpouching of bladder
3) Adenocarcinoma of the bladder

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30
Q

What is the Vitelline duct?

What pathology is seen with it?

A

It connects the yolk sac to the midgut lumen

1) Meckel’s diverticulum
2) Vitelline fistula –> meconium discharge from umbilicus

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31
Q

What is derived from the 1st aortic arch?

A

Maxillary artery

MS CARD

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32
Q

What is derived from the 2nd aortic arch?

A

Stapedial artery & hyoid artery

MS CARD

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33
Q

What is derived from the 3rd aortic arch?

A

Common Carotid & part of internal Carotid

MS CARD

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34
Q

What is derived from the 4th aortic arch?

A

Aortic arch & proximal R. subclavian

MS CARD

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35
Q

What is derived from the 5th aortic arch

A

Nothing (regresses)

MS CARD

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36
Q

What is derived from the 6th aortic arch?

A

Ductus arteriosus & proximal pulmonary artery

MS CARD

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37
Q

What types of tissue is the branchial (pharyngial) apparatus composed of?

A

Clefts - Ectoderm
Arches - Mesoderm
Pouches - Endoderm

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38
Q

What do the branchial clefts develop into?

A

1st cleft –> EAM

All others are obliterated. If one is not –> branchial cleft cyst within lateral neck

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39
Q

What is derived from the 1st pharyngeal (branchial) arch?

A 
Meckel's cartilage
Mandible
Malleus & incus
Mandibular ligament
Muscles of mastication
Mylohyoid

Anterior belly of the digastric
Tensor tympani
Tensor veli palatini
The nerves required to chew (V2 & V3)

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40
Q

What is seen with failure of the 1st aortic arch to develop properly?

A

Neural crest fails to migrate –> Treacher Collins syndrome

Symptoms:
Mandibular hypoplasia
Facial abnormalities

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41
Q

What is derived from the 2nd pharyngeal (branchial) arch?

A 
Stapes
Styloid
leSSer horn of hyoid
Stapedius muscle
Stylohyoid muscle
poSterior belly of the digastric

Seventh cranial nerve (CNVII)

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42
Q

What is derived from the 3rd pharyngeal (branchial) arch?

A

GlossoPHARYNGEAL nerve (CNIX)
Greater horn of hyoid
styloPHARYNGEOUS

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43
Q

What causes a congenital pharyngocutaneous fistula?

A

Persistent 3rd branchial cleft & pouch –> fistula to lateral neck

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44
Q

What is derived from the 4th pharyngeal (branchial) arch?

A

think swallowing

Superior laryngeal nerve (CNX)
Thyroid cartilage
Pharyngeal constrictor muscles
Cricothyroid muscle
Levator veli palatini muscle
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45
Q

What is derived from the 6th pharyngeal (branchial) arch?

A

think talking

Recurrent laryngeal nerve (CNX)
All laryngeal cartilages except thyroid cartilage (4th)
All intrinsic laryngeal muscles except cricothyroid

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46
Q

What is derived from the 1st branchial (pharyngeal) pouch?

A

Middle ear cavity
Mastoid air cells
Endoderm-lined structures of ear

Ear, Tonsils, bottom-To-top

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47
Q

What is derived from the 2nd branchial (pharyngeal) pouch?

A

Palatine tonsil epithelium

Ear, Tonsils, bottom-To-top

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48
Q

What is derived from the 3rd branchial (pharyngeal) pouch?

A

dorsal –> inferior parathyroids (bottom)
ventral –> thymus (to)

Ear, Tonsils, bottom-To-top

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49
Q

What is derived form the 4th branchial (pharyngeal) pouch?

A

Superior parathyroids (top)

Ear, Tonsils, bottom-To-top

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50
Q

What causes a cleft lip?

A

Maxillary & medial nasal processes do not fuse

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51
Q

What gene causes male development?

A

SRY gene –> Testis determining factor

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52
Q

What is derived from the mesonephric duct?

A

aka Wolffian duct –> SEED

Seminal vesicles
Epididymis
Ejaculatory duct
Ductus deferens

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53
Q

What is seen with congenital 5-alpha reductase deficiency?

A

Male internal genitalia
Ambiguous external genitalia until puberty
(DHT necessary)

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54
Q

What causes hypospadias?

A

Failure of urethral folds to close

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55
Q

What causes epispadias?

A

Faulty positioning of the genital tubercle

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56
Q

What is the lymphatic drainage of the vagina?

A

Proximal 2/3 –> obturator, external iliac, hypogastric nodes

Distal 1/3 –> superficial inguinal nodes

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57
Q

What ligament contains the ovarian vessels?

What does the ligament connect?

A

Suspensory ligament

Anchors ovaries to the lateral pelvic wall

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58
Q

What ligament contains the uterine vessels?

What does the ligament connect?

A

Cardinal ligament

Anchors the cervix to side wall of the pelvis

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59
Q

What ligament contains the Artery of Sampson?

What does the ligament connect?

A

Round ligament

Uterine fundus –> Labia majora

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60
Q

What ligament in the female pelvis travels through the inguinal canal?

A

Round ligament

Uterine fundus –> labia majora

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61
Q

What are the components of the broad ligament?

A

Mesometrium (lower portion)
Mesosalpinx (upper portion)
Mesovarium (lies on ovary)

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62
Q

What is connected by the ligament of the ovary?

A

Connects the ovary to the uterus

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63
Q

What is the pathway of sperm to exit the male?

A 
SEVEN UP:
Seminiferoustubules
Epididymis
Vas deferens
Ejactulatory duct
(Nothing)
Urethra
Penis
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64
Q

What nerves are responsible for the male sexual response?

A

Erection - pelvic nerve (parasympathetic)
Emission - hypogastric nerve (sympathetic)
Ejaculation - pudendal nerve

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65
Q

What is secreted by Sertoli cells?

A

Embryogenesis - Mullerian inhibitory factor

Adult:
Inhibin - feedback inhibition to FSH
Androgen binding protein - keep local [T] high

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66
Q

What forms the blood-testis barrier?

A

Tight junctions between Sertoli cells

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67
Q

How does increased temperature affect the testis?

A

Decreased sperm production
Decreased inhibin production
Normal testosterone production

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68
Q

What are the stages of sperm development?

What is their ploidy?

A

1) Spermatogonium (2n, 2c)
2) Primary spermatocyte (2n, 4c)
3) Secondary spermatocyte (1n, 2c)
4) Spermatid (1n, 1c)
5) Spermatozoa

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69
Q

What is spermatogenesis?

Spermiogenesis?

A

Spermatogenesis is the whole process

Spermiogenesis is spermatid –> mature spermatozoon

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70
Q

Where is aromatase found in adult males?

A

Leydig cells

Adipocytes

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71
Q

What is the relative potency of endogenous estrogens?

Where are they produced?

A

Estradiol > Estrone > Estriol

E2 = ovary
E1 = adipose
E3 = placenta
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72
Q

What is the effect of estrogen on lipoprotein levels?

A

^HDL

Decreased LDL

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73
Q

Describe Estrogen production in the ovary

A

LH stimulates theca cells –> Cholesterol –> Androstenedione via Desmolase

FSH stimulates granulosa cells –> Androstenedione –> Estrogen via Aromatase

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74
Q

How much estrogen is in a pregnant woman?

A

50x normal E2 & E1

1000x normal E3

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75
Q

What are the functions of progesterone?

A 
Stimulate endometrium (glands & spiral arteries)
Maintain pregnancy
Decrease myometrial excitability
Production of thick cervical mucus (inhibits sperm entry)
Increases body temperature
Inhibits gonadotropins
Relaxes uterine smooth muscle
Decreases estrogen receptor density
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76
Q

What are the Tanner stages of development?

A

I) Childhood

II) Pubic hair; breast bud

III) Pubic hair darkens & is curly; ^Penis length; ^Breast size

IV) ^Penis width; dark scrotal skin; raised areolae

V) Adult; areolae are not raised

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77
Q

What phase of the menstrual cycle varies from woman to woman?

A

The follicular phase varies

The luteal phase 14 days in all women.
Thus, ovulation + 14 days = menstruation

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78
Q

What is a normal menstrual cycle length?

A

21-35 days

35 = oligomenorrhea

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79
Q

What is menorrhagia?

Metrorrhagia?

A

Menorrhagia - heavy or prolonged bleeding

Metrorrhagia - irregular menstruation

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80
Q

Why is body temperature a marker for ovulation?

A

Ovulation –> corpus luteum releases progesterone –> ^temp

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81
Q

What is Mittelschmerz?

A

Rupture of a follicle –> small bleed into peritoneum –> irritation that can mimic appendicitis

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82
Q

When do oocytes undergo meiosis I & II?

A

Begin in utero
Arrested in prOphase of meiosis I until ovulation
Arrested in METaphase II until fertilization (it MET a sperm)

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83
Q

What are the stages of ovum development & their ploidy?

A

Oogonium (2n, 2c)
Primary oocyte (2n, 4c)
Secondary oocyte (1n, 2c)
Ovum (1n, 1c)

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84
Q

What is hCG detectable?

A 
In blood at 1 week
In urine (home test) at 2 weeks
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85
Q

When does hCG peak during pregnancy?

What secretes it?

A

Week 10

It is secreted by syncytiotrophoblasts

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86
Q

When does implantation of an embryo occur?

A

6 days after fertilization

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87
Q

What is the function of prolactin?

Oxytocin?

A

Prolactin - Induces/maintains lactation & inhibits GnRH

Oxytocin - Milk letdown & causes uterine contractions

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88
Q

Where is progresterone synthesized from during pregnancy?

A

1st trimester = corpus luteum (maintained by hCG)

2nd & 3rd trimesters = placenta

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89
Q

What causes Klinefelter’s syndrome?

What is seen?

A

XXY genotype

Testicular atrophy
Long extremities
Gynecomastia
Female hair distribution
Barr body (inactivated X chromosome in nucleus)
^FSH, ^LH, ^Estrogen, low Testosterone

Common cause of hypogonadism seen during an infertility workup.

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90
Q

What causes Turner syndrome?

What is seen?

A

XO genotype

Short stature
Streak ovaries
Shield chest w/ wide nipples
Bicuspid aortic valve
Preductal coarctation of the aorta
Horseshoe kidney
Cystic hygroma (webbed neck)
Lymphedema in hands/feet
Dysgerminoma
Short 4th digit

Most common cause of primary amenorrhea

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91
Q

What is the genetic cause of Turner syndrome (precisely)?

A 
60% = complete monosomy
30% = mosaicism
10% = structural abnormality of X chromosome
92
Q

What is seen in double Y males?

A

XYY genotype

Tall
Severe acne
Antisocial behavior
Autism spectrum disorders

93
Q

What causes female pseudohermaphroditism?

A

Ovaries present (XX) but external genitalia are virilized or ambiguous

Caused by inappropriate exposure to androgens during early gestation

94
Q

What causes male pseudohermaphroditism?

A

Testes present (XY) but external genitalia are female or ambiguous

Most common cause if androgen insensitivity syndrome

95
Q

What is seen with true hermaphroditism?

A

46XX or 47XXY

Both ovary and testicular tissue present. Ambiguous genitalia. This is very rare.

96
Q

What causes androgen insensitivity syndrome?

What is seen?

A

X-linked defect in the androgen receptor (46XY)

Female appearance
Vagina ends in blind pouch
No sexual hair
Testes present inside (removed to prevent malignancy)
^Testosterone, ^Estrogen, ^LH
97
Q

What is seen in 5-alpha reductase deficiency?

A

Autosomal recessive inheritance

Ambiguous genitalia until puberty (^T causes masculinization)
Everything else is normal (hormone levels, internal genitalia)

98
Q

What causes Kallmann syndrome?

What is seen?

A

Defective migration of GnRH cells & formation of olfactory bulb

Lack of secondary sex characteristics (male or female)
Anosmia
Low GnRH, LH, FSH, sex hormones

99
Q

What symptoms are indicative of a hydatidiform mole?

What will be seen with labs/US?

A 
Amenorrhea
Abnormal vaginal bleeding
Enlarged uterus (complete)
"Snowstorm" appearance on US (complete)
^hCG
100
Q

How are complete moles formed?

A

1 sperm + 1 empty egg –> replication –> 46XX
or
2 sperm + 1 empty egg –> 46XX/46XY

101
Q

How is a partial mole formed?

A

2 sperm + 1 egg –> 69XXY/69XXX/69XYY

102
Q 
What is the difference between complete & partial mole with regard to:
hCG
Uterine size
Risk of choriocarcinoma
Fetal parts
A

hCG: Complete^^^ Partial^
Uterine size: Complete^ Partial = normal
Risk of choriocarcinoma: Complete = 2 Partial = rare
Fetal parts: Only in partial

103
Q

What is the treatment of a hydatidiform mole?

A

Methotrexate + D&C

Monitor hCG for reemergence and for choriocarcinoma

104
Q

What causes preeclampsia?
What is seen?
What is seen in eclampsia?

A

Impaired vasodilation of spiral arteries –> placental ischemia –> increased systemic maternal vascular tone

Preeclampsia = Hypertension, proteinuria, edema
Eclampsia = Preeclampsia + seizures
105
Q

When does preeclampsia occur?

A

20 weeks to 6 weeks postpartum

If earlier than 20 weeks –> mole

106
Q

What are the risk factors for preeclampsia?

What is the incidence?

A

Occurs in 7% of pregnancies

Risk factors:
Preexisting hypertension
Diabetes
Chronic renal disease
Autoimmune disorders
107
Q

What are the clinical symptoms of preeclampsia?

A 
Headache
Blurred vision
Abdominal pain
Edema of face & extremities
Altered mental status
Hyperreflexia
Labs: Thrombocytopenia or hyperuricemia
108
Q

What is the treatment for preeclampsia/eclampsia?

A

Delivery of fetus as soon as viable
Bed rest, monitoring, treatment for HTN (methyldopa)

If seizures present - IV magnesium sulfate

109
Q

What is seen with placental abruption?

What can occur?

A

Abrupt detachment of placenta from decidua

Painful bleeding in 4rd trimester
Can cause shock, DIC, loss of fetus

110
Q

What are the risk factors for placental abruption?

A

Smoking
Hypertension
Cocaine use

111
Q

What causes placenta accreta?

What is seen?

A

Defective decidua –> placenta implants into myometrium

Massive bleeding seen after delivery. Often requires hysterectomy.

112
Q

What are the risk factors for placenta accreta?

A

Prior C-section
Inflammation (PID)
Placenta previa

113
Q

What is seen in HELLP syndrome?

What are the complications?

A

Hemolysis
Elevated Liver enzymes
Low Platelets

Risk of ARDS or cerebral hemorrhage

Often seen in conjunction with preeclampsia

114
Q

What is seen with teratogen exposure in utero based on the point in gestation?

A

Weeks 1-2 –> spontaneous abortion
Weeks 3-8 –> organ malformation
After week 9 –> organ hypoplasia

115
Q

What is seen with placenta previa?

What are the risk factors?

A

Placenta attaches to lower uterine segment –> painless bleeding at any point in pregnancy

Risk factors:
Multiparity
Prior C-section

116
Q

Where is the most common site for an ectopic pregnancy?

What is seen?

A

Fallopian tubes

Presents with Hx of amenorrhea + sudden lower abdominal pain
Low hCG based on dates
Dx confirmed with US

117
Q

What are the risk factors for ectopic pregnancy?

A 
History of infertility
Salpingitis (PID)
Ruptured appendix
Prior tubal surgery
Endometriosis

Basically anything that can scar the abdominal cavity

118
Q

What are the risk factors for SIDS?

A

SIDS = death of a healthy infant 1m-1y old

Smoking in household
Sleeping on stomach
Prematurity

119
Q

How does p53 cause apoptosis?

A

If DNA damage is deemed irreparable –> activates Bax –> binds up Bcl-2 –> permeable mitochondrial membrane –> cytochrome C –> apoptosis

120
Q

What is the mechanism of Rb as a tumor suppressor gene?

A

Rb binds E2F (transcription factor) & must be phosphorylated to release it –> progression in the cell cycle

When Rb is mutated, E2F is free

121
Q

What are the chances of CIN reversing in the cervix?

A

CIN1 –> 66%
CIN2 –> 33%
CIN3 –> Rare
CIS –> never

122
Q

What is a normal volume of amniotic fluid?

What can cause abnormal volumes?

A

0.5-1.5L

oligohydramnios (placental insuff., b/l renal agenesis, posteior urethral valves in males; can lead to Potter’s syndrome)

> 1.5L –> polyhydramnios (atresia, anencephaly)

123
Q

What are the stages of the menstrual cycle?

What stages do they correspond to in the ovulatory cycle?

A

1) Proliferative (Follicular phase; E2)
2) Secretory (Luteal phase; Progesterone)
3) Menstruation

124
Q

What causes Asherman syndrome?

What is seen?

A

Overaggressive D&C –> loss of basalis layer (stem cells) –> secondary amenorrhea

125
Q

When are anovulatory cycles seen?

A

Menarche & menopause typically

Common cause of dysfunctional uterine bleeding during these times.

126
Q

What causes CIN?

A

HPV 16, 18, 31, 33 infection

Normally cleared by the immune system. Persistent chronic infection can lead to CIN.

127
Q

What virulence factors of HPV lead to CIN?

A

Only found in HPV 16, 18, 31, 33. These strains have both factors.

E6 –> inactivates p53
E7 –> inactivates Rb

128
Q

What are the risk factors for cervical carcinoma?

A

Multiple sexual partners!!!
Smoking
Early age of 1st intercourse
HIV infection (AIDS-defining illness)

129
Q

What is seen on an abnormal Pap smear?

A

Koilocytes:
Large nucleus
Irregular (“rasinoid”) nucleus
Perinuclear halo

130
Q

What types of cervical carcinoma are possible?

A

SCC (80%)
Adenocarcinoma (15%)

Pap smear does not pick up adenocarcinoma very well. This type has not gone down in incidence.

131
Q

What is seen clinically in cervical carcinoma?

What complications are seen?

A

Bleeding
Postcoital bleeding
Generally in middle-aged females (takes years to develop)

Complications:
Lateral invasion into bladder –> blocks ureters –> postrenal kidney failure
Rarely metastasizes

132
Q

What are the causes of endometritis?

How is it treated?

A

Retained products of conception (no matter the outcome)
IUD

Tx: Gentamycin + Clindamycin +/- Ampicillin

133
Q

What symptoms are seen with endometriosis?

A 
Menorrhagia
Dysmenorrhea
Dyspareunia
Infertility
Pain w/ defecation or urination
134
Q

What is the treatment for endometriosis?

A

OCP’s
NSAIDs
Leuprolide
Danazol

135
Q

What is seen with adenomyosis?

What is the treatment?

A

Caused by endometrium within the myometrium

Menorrhagia
Dysmenorrhea
Pelvic pain
Enlarged uterus

Tx: Hysterectomy

136
Q

What causes Cowden syndrome?

What is seen?

A

Germline PTEN mutation

GI & skin hamartomas
Macrocephaly
Breast, thyroid, endometrial carcinoma

137
Q

What is extramammary Paget’s disease?

A

It is an intraepithelial adenocarcinoma of the vulva or penis. It does not indicate additional underlying cancer, as does Paget’s disease of the breast.

138
Q

What are the risk factors for endometrial hyperplasia?

How does it present?

A

Presents as postmenopausal bleeding.

Anovulatory cycles
HRT
PCOS
Granulosa-Theca cell tumor

All of these ^E2 exposure

139
Q

What is the best indicator of risk for endometrial hyperplasia to transform into endometrial carcinoma?

A

Atypia

140
Q

What are the risk factors for endometrial carcinoma?

A 
Estrogens w/out progestins
Nulliparity
Late menopause
Obesity
Diabetes
HTN
141
Q

What are the subtypes of endometrial carcinoma?

A

Endometrioid = 80% (arises from endometrial hyperplasia; PTEN)

Serous/Papillary = 20% (p53)

142
Q

How does leiomyosarcoma differ from leiomyoma?

A

Leiomyosarcoma:
Single tumor
Irregularly shaped w/ necrosis & hemorrhage
Seen in postmenopausal women

***DOES NOT ARISE FROM LEIOMYOMA

143
Q

What is the most common tumor overall in females?

A

Uterine fibroids (leiomyoma)

More common in blacks

144
Q

What is seen clinically with uterine fibroids?

A 
Leiomyomas:
Present in 20-40y women (E2 sensitive)
Usually asymptomatic
Abnormal uterine bleeding
Miscarriage
145
Q

What is considered premature ovarian failure?

A

Before age 40

146
Q

What is the DDx for anovulation?

A 
Pregnancy
PCOS
Obesity
HPO axis abnormalities
Eating disorders
Premature ovarian failure
Hyperprolactinemia
Thyroid disorders
Cushing's syndrome
Adrenal insufficiency
147
Q

What is the pathophysiology of PCOS?

A

^LH –> ^Androgens –> ^Estrone (aromatized in fat) –> Feeds back to decrease FSH –> No ovulation –> Cysts & infertility

Also the high levels of androgens cause hirsutism.

148
Q

What other conditions are associated with PCOS?

A 
Insulin resistance --> development of T2DM
Endometrial cancer (high estrogen)
149
Q

How does PCOS present clinically?

What are the relative hormone levels?

A

Amenorrhea
Infertility
Obesity
Hirsutism

High LH, Testosterone, Estrogen
Low FSH

150
Q

How is PCOS treated?

A 
Weight loss
Low dose OCP or medroxyprogesterone
Spironolactone (for hirsutism & acne)
Clomiphene (if pregnancy desired)
Metformin (often enough to regain fertility)
151
Q

What is the most common ovarian mass in a young woman?

A

Follicular cyst (unruptured Graafian follicle)

152
Q

What categories of ovarian tumors are most common to what age groups?

A

Children & young women (0-30) –> germ cell tumors

Middle-aged (30-50) –> benign surface epithelial tumor

Older (50-80) –> malignant surface epithelial tumor

153
Q

What tumor markers are associated with dysgerminoma?

Who is at risk?

A

Female version of seminoma

hCG and/or LDH may be elevated

Associated with Turner syndrome

154
Q

What accounts for the difference in prognosis between gestational choriocarcinoma and germ cell choriocarcinoma?

A 
Germ cell (ovarian) --> No response to chemo
Gestational --> Very chemosensitive

Also germ cell choriocarcinoma shows early hematogenous spread to the lungs.

155
Q

What are the relative [hCG] of pregnancy and gestational trophoblastic disease?

A

Choriocarcinoma > Complete mole > Partial mole > Pregnancy

156
Q

What tumor marker is seen with endodermal sinus tumors?

What is seen histologically?

A

aka Yolk sac tumors (seen in testis & ovaries)

AFP is tumor marker

Schiller-Duval bodies present –> resemble glomeruli

157
Q

What germ cell tumor is seen largely in young children?

A

Endodermal sinus tumors (yolk sac tumors)

Applies to both males & females

158
Q

What is the most common ovarian germ cell tumor?

A

Teratoma (90% of germ cell tumors)

159
Q

What is Struma ovarii?

A

Immature teratoma composed of functional thyroid tissue –> hyperthyroidism

160
Q

What tumor marker is used for ovarian surface epithelial tumors?

A

CA-125

Good to monitor progression & recurrence, not for screening.

161
Q

What type of ovarian tumor is BRCA associated with?

A

Most commonly serous cystadenoma/cystadenocarcinoma

BRCA1 > BRCA2 > HNPCC

Family history is the most important risk factor

162
Q

What is pseudomyxoma peritonei?

A

A mucinous tumor (appendix > ovarian) causes accumulation of mucinous material within the peritoneum

163
Q

What does a Brenner tumor look like grossly?

Histologically?

A

Grossly - Yellow/tan, unilateral, encapsulated

Histology - Looks like urothelial tissue, “coffee bean nuclei”

164
Q

What is Meigs’ syndrome?

A

Triad of:
Ovarian fibroma tumor
Ascites
Hydrothorax

165
Q

What is seen clinically with a Granulosa-Theca cell tumor?

A

Estrogen secretion by tumor:
Precocious puberty in kids
Abnormal uterine bleeding
Endometrial hyperplasia/carcinoma

166
Q

What is seen histologically with Granulosa-Theca cell tumors?

A

Call-Exner bodies - small primitive follicles filled with eosinophilic secretions

“Call Granny”

167
Q

What is seen with a Krukenberg tumor?

A

Mucin secreting signet-ring cell gastric adenocarcinoma metastasizes to bilateral ovaries

168
Q

What are the staining patterns of extramammary Paget’s disease?
Melanoma?

A

Paget cells: PAS+, Keratin+, S100-

Melanoma: PAS-, Keratin-, S100+

169
Q

What is vaginal adenosis?

A

Persistence of columnar epithelium in the upper 1/3 of the vagina. Normally the columnar epithelium (Paramesonephric) is replaced by squamous epithelium (urogenital sinus).

Can occur spontaneously or (much more commonly) due to DES exposure in-utero –> ^risk of clear cell adenocarcinoma.

170
Q

What is seen in sarcoma botryoides?

A

Embryonal rhabdomyosarcoma presents as a grape-like mass protruding from the vagina or penis. It is seen in children <4y

171
Q

What is seen on histology of sarcoma botryoides?

A

Cytoplasmic cross-striations

Positive staining for desmin & myoglobin (skeletal muscle origin)

172
Q

What is ovarian caking?

A

Ovarian cancer seeds the omentum & appears cake-like.

173
Q

What are the risk factors for ovarian cancer?

What is associated with lower risk?

A

BRCA1, BRCA2, HNPCC

OCP’s lower risk
Multiparity & breastfeeding lower risk
This is because less ovulation –> less regeneration & chance for error

174
Q

What is the histology of normal breast tissue?

A

Inner luminal layer
Outer myoepithelial layer

This is present in both the lobules & ducts.

175
Q

What are the benign breast tumors?

A

Fibroadenoma
Intraductal papilloma
Phyllodes tumor

176
Q

What is seen with a fibroadenoma?

What is the associated risk of breast cancer?

A

Most common breast tumor in pre-menopausal women
Small, mobile, firm mass with sharp edges
^size & tenderness with estrogen (pregnancy, menstruation)

No increased risk of breast cancer

177
Q

How does intraductal papilloma present?

What is the risk of breast cancer?

A

Bloody nipple discharge (usually in young woman)
Typically grows beneath areola & has 2 normal cell layers

Slight (2x) increased risk for breast cancer

178
Q

What is seen histologically with Phyllodes tumor?

What is the risk for breast cancer?

A

Bulky mass of fibrous tissue & cysts
“Leaf-like” projections
Seen in 6th decade

Some may become malignant (vs. fibroadenoma)

179
Q

With regard to breast cancer, what does nipple inversion signify?
Skin dimpling?

A

Nipple inversion –> has invaded central breast

Skin dimpling –> infiltration of suspensory Cooper ligaments

180
Q

What is a sentinel lymph node biopsy?

A

Initially biopsy only the sentinel lymph nodes (the first ones that lymph will encounter). If they are positive for cancer, then excise all of the LN’s. If they are negative, you are good.

181
Q

What group is at risk for triple negative breast cancer?

What is the association with prognosis?

A

Black women –> ER-, PR-, HER-

It is a poor prognosis.

182
Q

What cancers are seen with BRCA1 & BRCA2 mutation?

A

BRCA1 - Breast (medullary^), Ovarian (serous)

BRCA2 - breast carcinoma in males

183
Q

What are the risk factors for male breast cancer?

A

BRCA2

Klinefelter’s syndrome

184
Q

What are the subtypes of mastitis?

What are their causes?

A

Acute mastitis:
Breastfeeding –> S. aureus infection

Periductal mastitis:
Smoking –> relative Vit. A deficiency –> squamous metaplasia in lactiferous ducts –> keratin plugging –> inflammation

185
Q

How do the subtypes of mastitis present?

A

Acute mastitis - redness & inflammation in a breastfeeding mom

Periductal - subareolar mass with nipple retraction

186
Q

Green-brown nipple discharge

A

Mammary duct ectasia

Secondary to inflammation & dilation of subareolar duct. Arises in multiparous postmenopausal woman (must DDx from breast cancer).

187
Q

What is comedocarcinoma?

What is seen on histology?

A

Comedocarcinoma is a subtype of DCIS

Caseous necrosis seen in the center of the duct with dystrophic calcification of the necrotic tissue. Surrounded by cancer cells.

188
Q

What is the most common type of breast cancer?

A

Invasive ductal carcinoma

Also the worst prognosis

189
Q

What is seen on histology of invasive lobular carcinoma?

A

Orderly single file cells

This is because E-cadherin is mutated early so the cells can lose their architecture. Often multifocal & seen bilaterally.

190
Q

What is seen on histology with medullary breast carcinoma?

What is the prognosis?

A

Subtype of ductal carcinoma
Lymphocytic infiltrate

Has a good prognosis

191
Q

What is seen with inflammatory breast carcinoma?

What is the prognosis?

A

Peau d’orange
Invasion of dermal lymphatics by the breast carcinoma

Subtype of ductal carcinoma with a poor prognosis

192
Q

What causes mammary Paget’s disease?

A

Paget cells within the epidermis (large cells w/ nuclear halo)

Indicates DCIS that has extended along the duct to the nipple.

193
Q

What is seen on staining for HER-2?

ER/PR?

A

Her-2 –> cell surface stains positive (EGFR tyrosine kinase rec.)

ER/PR –> nucleus stains positive (translocate to nucleus upon binding the hormones)

194
Q

How does fibrocystic disease present?

A

Lumpy breasts in a young woman
Premenstrual breast pain & fluctuation of size
Often bilateral

195
Q

What are the histologic types of fibrocystic change & their relative chances of developing cancer?

A

Nonproliferative (blue dome cysts, apocrine metaplasia, fibrosis) –> no ^ risk

Hyperplasia w/ no atypia --> 2x ^ risk
Sclerosing adenosis (calcifications & ^ # of acini) --> 2x ^ risk

Prolferative w/ atypia –> 5x risk

CIS –> 10x risk

196
Q

How does fat necrosis of the breast occur?

A

Painless lump following trauma (usually can’t recall)

Calcified (saponification) on mammography

197
Q

What can cause gynecomastia?

A

Hyperestrogenism (cirrhosis, tumor, puberty, old age)
Klinefelter’s syndrome
Illicit drugs
Spironolactone, Digitalis, Cimetidine, Alcohol, Ketoconazole
(Some Drugs Create Awkward Knockers)

198
Q

What other embryologic abnormality is epispadias associated with?

A

Bladder exstrophy

Bladder wall exposed out of the abdominal wall.

199
Q

What causes lymphogranuloma venereum?

A

Chlamydia trachomatis L1-L3

200
Q

What are the precursor lesions to penile SCC?

A

Bowen disease - leukoplakia on the shaft

Erythroplasia of Queyrat - erythroplakia on glans

Bowenoid papulosis - reddish papules (doesn’t invade)

201
Q

What organs can be inflamed due to mumps?

A

Parotitis
Orchitis
Meningitis

Your balls get as big as POM POMs

202
Q

What lobes are affected by BPH?

Prostate cancer?

A

BPH - periurethral (middle & lateral) lobe

Cancer - peripheral (posterior) lobe

203
Q

What are the pharmacologic treatments for BPH?

A

Alpha1 antagonists (Terazosin, tamsulosin)

5-alpha-reductase inhibitors (Finasteride)

204
Q

What PSA level is typically seen in BPH?

Prostatic adenocarcinoma?

A 
BPH = 4-10
Cancer = > 10
205
Q

What tumor markers are used for prostate cancer?

A 
PSA
Prostatic acid phosphatase (PAP)
Alkaline phosphatase (if mets to bone)
206
Q

What sequelae can result from cryptorchidism?

A

Infertility
Germ cell tumors (seminoma)
Low testosterone (if bilateral)

207
Q

How does a seminoma present grossly?

Histologically?

A

Gross: Homogenous, no necrosis, no hemorrhage

Histo: Fried egg appearance

208
Q

What tumor markers are elevated in seminomas?

A

hCG (sometimes)

Placental alkaline phosphatase (PLAP)

209
Q

What is the prognosis of a seminoma?

A

Radiosensitive
Late mets
Excellent prognosis

210
Q

What germ cell tumor may produce paraneoplastic syndromes?

A 
Immature teratoma (females):
Struma ovarii --> Hyperthyroidism

Choriocarcinoma (hCG):
Hyperthyroidism
Gynecomastia in males

hCG at high concentrations binds TSH & LH receptors

211
Q

What is the prognosis of teratomas?

A

In females –> usually mature & benign

In males –> even mature ones are malignant

212
Q

What serum markers are elevated in teratomas?

A

Male - possibly AFP or hCG

213
Q

Why are testicular tumors not biopsied?

A

~90% are germ cell tumors –> malignant

Also, biopsy could seed the scrotum

214
Q

What are the testicular germ cell tumors?

A 
Seminoma
Endodermal sinus (yolk sac)
Choriocarcinoma
Teratoma
Embryonal carcinoma
215
Q

What is grossly with a Leydig cell tumor?

Histologically?

A

Grossly - Golden brown color

Histo - Reinke crystals

216
Q

What is the most common testicular cancer in older men?

A

Metastatic DLBC lymphoma

Usually bilateral

217
Q

What causes a hydrocele?

A

Incomplete closure of the processus vaginalis

218
Q

What are the antiandrogens?

A

Finasteride (5-alpha-reductase inhibitor)
Flutamide (androgen antagonist)
Ketoconazole (inhibits 17-alpha-hydroxylase)
Spironolactone (inhibits steroid binding)

219
Q

What are the SERMs?

A

Clomiphene
Tamoxifen
Raloxifene

220
Q

What is the mechanism of Clomiphene?

Toxicities?

A

Partial agonist at ER in hypothalamus (SERM) –> prevents normal feedback inhibition –> ^GnRH release

Toxicities:
Hot flashes
Multiparity
Visual disturbances

221
Q

What is Raloxifene used for?

A

Treats osteoporosis

Agonist on bone
Antagonist on uterus & breast

222
Q

What are the aromatase inhibitors?

What are they used for?

A

Anastrozole (reversible)
Exemestane (irreversible)

Used in ER+ breast cancer in postmenopausal women.

223
Q

What is the mechanism of Mifepristone?
What is it used for?
What are the side effects?

A

Mifepristone is a progesterone antagonist –> abortion
It is administered with Misoprostol (PGE1)

Side effects:
Heavy bleeding
N/V
Abdominal pain

224
Q

What are the contraindications of OCP’s?

A

Smokers > 35y
Hx of thromboembolism
Hx of estrogen-dependent tumor

225
Q

What is Tamsulosin?

What is its use?

A

Selective Alpha-1a/d agonist used to treat symptoms of BPH by relaxing smooth muscle contraction

Alpha1b = vascular receptors

226
Q

What toxicities are seen with Sildenafil/Vardenafil?

A

Headache
Flushing
Blue/green vision changes
Life-threatening hypotension if taken with nitrates

227
Q

What is Danazol?

What are its uses?

A

Synthetic androgen partial agonist

Used for endometriosis & hereditary angioedema

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