A HY Review of The Reproductive

System
Some MS4
Introduction/Objectives
-Welcome to Repro. In its own way, it is a “fun” block (you know how…..)

-Repro is a nice continuation from Endocrine. I’d recommend going back to review the
endocrine stuff since it’s still fresh. It will be 1 less thing to worry about wrt Step 1
studying.

-There’s tons of problems (46) in these slides presented as clinical vignettes with
aftermath slides that provide solutions and the reasoning behind many of these
solutions. I’ll spend a lot of the session on the whiteboard trying to drive key points
home. My primary goal with these vignettes is to point out the classic “exam”
presentations of OB GYN pathologies. You should definitely pay attention to them.

-If you’ve not started studying for Step 1, its not too late. Start making a nice pass
through first aid. Spend time understanding the material (especially your weak spots)
so you’ll go into review mode during your dedicated period.
Q1
17 yo F has never had menses, has Tanner 5 breasts, normal external female genitalia,
and has scant pubic/axillary hair. Pelvic US reveals no uterus/ovaries and bilateral
undescended testes.

What is the most likely dx?

Why does this patient have a vagina? Normal female external genitalia? Breasts?

Why does this patient lack a uterus/fallopian tubes?

Why does she lack pubic/axillary hair?

What should be true of testosterone and LH levels in this patient?

Q1 Key
17 yo F has never had menses, has Tanner 5 breasts, normal external female genitalia,
and has scant pubic/axillary hair. Pelvic US reveals no uterus/ovaries and bilateral
undescended testes.

What is the most likely dx?-Androgen Insensitivity Syndrome (AIS) secondary to

testosterone receptor mutations. Individuals are 46 XY but are phenotypically female.

Why does this patient have a vagina? Normal female external genitalia? Breasts?

Vagina/normal female genitalia-default program for the external genitalia (lower

vagina, labia majora/minora) is female with DHT required for development toward the
penis/prostate pathway.

Breasts-testosterone can be aromatized (aromatase, inhibited by Anastrozole,

Exemestane) to estrogen which will drive breast development.
Q1 Key contd.
Why does this patient lack a uterus/fallopian tubes?-Sertoli cells in the testes make
MIF (or AMH, your pick) which nukes the mullerian (paramesonephric) duct in utero
and its associated derivatives (uterus, fallopian tubes, NOT OVARIES!). She has no
ovary b/c she is not female.

Why does she lack pubic/axillary hair?-testosterone is needed for pubic/axillary hair
development (and also body odor).

What should be true of testosterone and LH levels in this patient?-Defective

testosterone (T) receptors in the anterior pituitary impair negative feedback, leading to
high LH and thus T levels.
Normal Male Sexual Development
Normal Male/Female Sexual Development
Q2
A 53 yo F presents to her PCP for an annual checkup. She has had DM for 10 years that
is well controlled with metformin. She has not had menses in the past 19 months.
Sexual intercourse with her husband is occasionally painful. Every few days she has 3-4
episodes of 5 min “heat strokes”.

What is your diagnosis?

What is considered a premature form of this phenomenon?

What should be true of FSH levels?

What are the 3 kinds of estrogens? At this patient’s age, what is the predominant kind
of estrogen?
Q2 Key
A 53 yo F presents to her PCP for her annual checkup. She has had DM for 10 years that is
well controlled with metformin. She has not had menses in the past 19 months. Sexual
intercourse with her husband is occasionally painful. Every few days she has 3-4 episodes of
5 min “heat strokes”.

What is your diagnosis?-Menopause (average age in the US is 51).

What is considered a premature form of this phenomenon?-premature ovarian

failure-stopping menses at an age < 40. This is pathologic.

What should be true of FSH levels?-elevated. With no follicles, inhibin and progesterone are
no longer released so negative feedback at the AP is gone.

What are the 3 kinds of estrogens? At this patient’s age, what is the predominant kind of
estrogen (estrone)?-Estradiol/E2 (prior to menopause, nonpregnant), Estriol (pregnancy,
from fetal DHEAS), Estrone (after menopause, from aromatization in adipocytes).
Q3-Hormone Festival
Increases milk production
Increases milk letdown
“Invigorates” uterine contractions
Plays a role in gestational DM
Maintains corpus luteum
Maintains pregnancy for first 10 weeks
Converts endometrium from being proliferative to being secretory
Causes endometrial hyperplasia
Thickens cervical mucus
Causes growth of the ovarian follicle
Causes ovulation
Prevents lactation during pregnancy-progesterone (blunts prolactin effect)
Hormone in highest concentration in the luteal phase of the menstrual cycle-progesterone
Produced by theca cells
Produced by granulosa cells
2 hormones produced by sertoli cells
Hormone produced by leydig cells
Inhibits FSH release from the anterior pituitary
Q3 Key-Hormone Festival
Increases milk production-prolactin
Increases milk letdown-oxytocin
“Invigorates” uterine contractions-oxytocin
Plays a role in gestational DM-human placental lactogen
Maintains corpus luteum-beta-HCG
Maintains pregnancy for first 10 weeks-progesterone from corpus luteum
Converts endometrium from being proliferative to being secretory-progesterone
Causes endometrial hyperplasia-estrogen (estriol in pregnancy)
Thickens cervical mucus-progesterone
Causes growth of the ovarian follicle-FSH
Causes ovulation-LH
Prevents lactation during pregnancy-estrogen/progesterone (blunts prolactin effect)
Hormone in highest concentration in the luteal phase of the menstrual cycle-progesterone
Produced by theca cells-androstenedione
Produced by granulosa cells-estrogen (type depends on age)
2 hormones produced by sertoli cells-Anti-Mullerian Hormone (AMH), Inhibin
Hormone produced by leydig cells-testosterone
Inhibits FSH release from the anterior pituitary-Inhibin
Q4
A 23 yo F presents to an obstetrics specialist for her annual OB visit. A routine pap
smear conducted reveals high grade precancerous lesions at the squamocolumnar
junction.

What is your dx?

What is the strongest risk factor for this patient’s condition?

How can this condition be prevented?

What is the most common cancerous lesion associated with this condition?
Q4 Key
A 23 yo F presents to an obstetrics specialist for her annual OB visit. A routine pap
smear conducted reveals high grade precancerous lesions at the squamocolumnar
junction.

What is your dx?-Cervical Intraepithelial Neoplasia (CIN). Could be LSIL (CIN 1,

basal ⅓) or HSIL (CIN 2 or 3, add progressive thirds from the bottom). Tx is with
LEEP, electrocautery, etc.

What is the strongest risk factor for this patient’s condition?-HPV 16, 18, 31 (from
E6/E7 expression). Don’t forget HPV 6/11 with genital warts.

How can this condition be prevented?-HPV vaccination.

What is the most common cancerous lesion associated with this condition?-Squamous
cell carcinoma. (Re-adenocarcinoma for the endocervix, think embryology).
Q5
33 yo F presents to her PCP with a 4 yr hx of irregular menses. BMI is 33.

What is your diagnosis?

What is your first diagnostic test?

What are the 3 criteria that suggest the dx of this disorder?

What should be seen on a transvaginal US?

What should be true of estrogen, testosterone, and LH levels in this patient?

What are some classic associations with this condition in terms of BMI, blood glucose
levels, and PE findings?
Q5 Key
33 yo F presents to her PCP with a 4 yr hx of irregular menses. BMI is 33.

What is your diagnosis?-Polycystic Ovarian Syndrome (PCOS)

What is your first diagnostic test?-Urine Pregnancy Test (why???)

What are the 3 criteria that suggest the dx of this disorder?-polycystic ovaries on US, signs
of androgen excess (e.g. hirsutism), and anovulation.

What should be seen on a transvaginal US?-polycystic ovaries (duh!)

What should be true of estrogen, testosterone, and LH levels in this patient?-all elevated.

What are some classic associations with this condition in terms of BMI, blood glucose
levels, and PE findings?-obesity (BMI > 30), insulin resistance (elevated BG), acne/hirsutism
(from too much testosterone/DHT) AND acanthosis nigricans (insulin resistance as well).
Q6
Supply the right intervention to the following parameters in the patient from Q5.

Fasting blood glucose of 210 mg/dl

Is tired of being hirsute

Improve menstrual regularity

Desires kids

For patients with PCOS, what are we most worried about from a malignancy
standpoint?

What would the results of a test (in a patient with PCOS) be with administration of
progesterone and subsequent withdrawal?
Q6 Key
Supply the right intervention to the following parameters in the patient from Q5.

Fasting blood glucose of 210 mg/dl-exercise, weight loss, metformin (very HY!)

Is tired of being hirsute-spironolactone (androgen receptor blocker/skin 5AR inhibitor)

Improve menstrual regularity-combination OCPs (nuke GnRH/FSH/LH, provides progesterone

for “withdrawal menstruation”).

Desires kids-clomiphene (SERM, blocks E2 receptors in the hypothalamus which releases GnRH
-ve feedback, upregulates the HPG axis).

For patients with PCOS, what are we most worried about from a malignancy
standpoint?-endometrial hyperplasia/carcinoma.

What would the results of a test (in a patient with PCOS) be with administration of progesterone
and subsequent withdrawal?-withdrawal bleed (why??). HY to understand this for tests.
Some Thoughts On PCOS-Pathophysiology
-There’s some “hand waving” on exactly what causes PCOS so here’s what I think (a lot of
this stuff is true though).

-There’s a “steady state” LH release. In other words, LH is released at a fairly constant level
with little to no variation. With no variation in this “constant”, there is no such thing as an
“LH surge” so ovulation never happens.

-Since ovulation never happens, progesterone levels will be down. The constant LH release
will lead to theca cell stimulation with a concomitant release of androgens.

-These androgens can take 2 pathways (DHT is one). The second pathway is aromatization
to estrogen which gives rise to unopposed E2 effects on the endometrium which causes
endometrial hyperplasia (and if left for long-endometrial cancer).

-Hyperinsulinemia is a common finding in PCOS. There’s very good research supporting

insulin’s role as a 5-alpha reductase activator.
Some Thoughts On PCOS-Pathophysiology contd.
-By activating 5-alpha reductase, T is converted to DHT. DHT promotes the formation
of “male pattern hair” which is observed as hirsutism.

-Insulin has also been found to be a theca cell stimulator which may also explain the
high androgen levels.

-High T levels decrease serum levels of SHBG. With less SHBG, less T is bound up, so
free T levels increase which basically creates a self feeding cycle.

-Having this mental framework should then help you visualize why metformin
(increases insulin sensitivity), spironolactone (androgen receptor blocker, 5-alpha
reductase inhibitor), clomiphene (SERM at hypothalamus, restores GnRH pulsatility
so FSH is released, basically normalizing the HPG axis), and OCPs (inhibit
gonadotropin release at the pituitary) help target these disparate pathways that play a
role in the different findings with PCOS.
Q7
Match the clinical description to the most likely diagnosis;

17 yo F presents with frothy, foul smelling, vaginal discharge. Pelvic exam reveals red
punctations on the cervix.

17 yo F presents with a colorless, foul smelling, vaginal discharge. Microscopic analysis

reveals “clue cells”.

17 yo F presents with a white, curdy/lumpy vaginal discharge, vaginal pH is < 4.5

Q7 Key (Very HY!)
Match the clinical description to the most likely diagnosis;

17 yo F presents with frothy, foul smelling, vaginal discharge. Pelvic exam reveals red
punctations on the cervix-Trichomonas Vaginalis, sexually transmitted, treatment is
with Metronidazole/MTZ (remember GET GAP on the METRO mnemonic).
Organisms are seen on microscopy with “wet prep” (normal saline).

17 yo F presents with a colorless, foul smelling, vaginal discharge. Microscopic analysis

reveals “clue cells”-Bacterial vaginosis, occurs secondary to vaginal flora disturbance
(normally Lactobacillus), treat with MTZ, +ve whiff test (fishy odor with KOH),
organisms seen with wet prep (NS).

17 yo F presents with a white, curdy/lumpy vaginal discharge, vaginal pH is <

4.5-candida vaginitis, “cottage cheese” vaginal discharge, pseudohyphae on microscopy,
treat with oral fluconazole, seen with KOH prep (not wet prep).
Common Vaginal Infections
Q8
Match the clinical description to the most likely diagnosis;

Baby born at 30 weeks gestation presents with dyspnea and respiratory distress. SaO2 is < 85%.
CXR reveals ground glass opacities.

Baby born at 30 weeks gestation has required intensive respiratory support. Neonate has been
irritable. Recent bowel movements have been bloody. Abdominal XR reveals air in the wall of the
bowel.

Baby born at 30 weeks gestation is discharged 5 weeks after delivery. He still requires home O2.

Baby born at 30 weeks gestation has required intensive respiratory support. He has the sudden
onset of nausea, vomiting, and headache. PE reveals a bulging fontanelle.

Baby born at 30 weeks gestation has required intensive respiratory support for the past 3 weeks. A
funduscopic exam reveals proliferative retinal changes with fragile blood vessels.
Q8 Key
Match the clinical description to the most likely diagnosis;

Baby born at 30 weeks gestation presents with dyspnea and respiratory distress. SaO2 is < 85%.
CXR reveals ground glass opacities-Respiratory distress syndrome (RDS). Note the classic CXR
(ground glass opacities, air bronchograms-note these buzzwords), tx is with CPAP but be careful.
Surfactant deficiency that can be obviated by prenatal corticosteroids (for step 1, remember
lamellar bodies as the source of surfactant in T2 pneumocytes and the L/S ratio being > 2).

Baby born at 30 weeks gestation has required intensive respiratory support. Neonate has been
irritable. Recent bowel movements have been bloody. Abdominal XR reveals air in the wall of the
bowel-Necrotizing Enterocolitis. Classic AXR finding of “pneumatosis intestinalis” (gas in bowel
wall). Bloody bowel movements. Look out for an AXR with straight lines in the wall of the bowel.

Baby born at 30 weeks gestation is discharged 5 weeks after delivery. He still requires home
O2-Bronchopulmonary Dysplasia (BPD), lung fibrosis secondary to O2 toxicity from intensive
respiratory support secondary to RDS. O2 requirement > 28 days after delivery.
Q8 Key contd.
Baby born at 30 weeks gestation has required intensive respiratory support. He has the
sudden onset of nausea, vomiting, and headache. PE reveals a bulging
fontanelle-intraventricular hemorrhage. Common comorbidity in the premature. Dx is
commonly with ultrasound OR CT scan. Presents with signs of increasing ICP. Call
neurosurgery.

Baby born at 30 weeks gestation has required intensive respiratory support for the past
3 weeks. A funduscopic exam reveals proliferative retinal changes with fragile blood
vessels-Retinopathy of prematurity. Arises secondary to hypoxic changes secondary to
RDS. Hypoxia induces aberrant blood vessel proliferation. Tx is with laser ablation.
Q9
Match the clinical description to the most likely diagnosis;

30 week old has had an unremarkable course since delivery. Newborn nursery exam 1
week after birth reveals a continuous, machine like murmur on auscultation. CXR
reveals increased pulmonary vascular markings.

Newborn presents with respiratory distress on delivery. PE reveals a “scaphoid”

abdomen (as a hint, most newborns have distended abdomens).
Q9 Key
Match the clinical description to the most likely diagnosis;

30 week old has had an unremarkable course since delivery. Newborn nursery exam 1
week after birth reveals a continuous, machine like murmur on auscultation. CXR
reveals increased pulmonary vascular markings-Patent Ductus Arteriosus (PDA).
Relatively common in preemies. Remember the ductus closes a few hours after birth.
Delivery on an accelerated schedule makes it very likely that the ductus stays open
longer than normal. Try indomethacin (prostaglandin synthesis inhibitor).

Newborn presents with respiratory distress on delivery. PE reveals a “scaphoid”

abdomen (as a hint, most newborns have distended abdomens)-Diaphragmatic hernia.
AXR will reveal bowel in the thorax. Next step is to intubate the child and call surgery.
For step 1, remember EA with a TE fistula when a Q stem describes drooling with the
first feed.
Q10-Pharm Quick Hits
Treats fertility, prostate cancer, and constitutional precocious puberty
Long term tx option for BPH/male pattern baldness, gynecomastia SE
Androgen receptor blocker, treats prostate cancer
Used to tx PCOS, 5-alpha reductase inhibitor, treats CHF
SERM used to treat PCOS
Estrogen agonist in endometrium, antagonist in breast
Estrogen antagonist (breast/endometrium), agonist in bone
Aromatase inhibitor, breast Ca tx in postmenopausal females
Immediate BPH relief, lowers BP
Immediate BPH relief, specific for prostate
Given to mom at risk for preterm delivery
Prevents uterine contractions
DOC in erectile dysfunction, cGMP inhibitor
Q10 Key-Pharm Quick Hits (commit to memory!)
Treats infertility, prostate cancer, and constitutional precocious puberty-leuprolide
(give continuously to kill fertility/prostate, give in pulsatile fashion for fertility).
Long term tx option for BPH/male pattern baldness, gynecomastia SE-finasteride
(5-alpha reductase inhibitor, prevents DHT formation).
Androgen receptor blocker, treats prostate cancer-Bicalutamide, Flutamide.
Used to tx PCOS, 5-alpha reductase inhibitor, treats CHF-Spironolactone.
SERM used to treat PCOS-Clomiphene (promotes pregnancy).
Estrogen agonist in endometrium, antagonist in breast-Tamoxifen.
Estrogen antagonist (breast/endometrium), agonist in bone-Raloxifene.
Aromatase inhibitor, breast Ca tx in postmenopausal females-Anastrozole.
Immediate BPH relief, lowers BP-Terazosin, Doxazosin.
Immediate BPH relief, specific for prostate-Tamsulosin (alpha 1-A,D blocker).
Given to mom at risk for preterm delivery-corticosteroids (surfactant help).
Prevents uterine contractions-tocolytics (ritodrine, terbutaline-beta 2 agonists).
DOC in erectile dysfunction, cGMP inhibitor-Sildenafil, Tadalafil (very HY drugs!)
Q11
Match the clinical presentation of primary amenorrhea to the most likely diagnosis;

20 yo F has breasts and a uterus, levels of all hormones are normal.

20 yo F supermodel (or hardcore athlete) has breasts and a uterus (what should be true of her
hormone levels?)

20 yo F has breasts and no uterus, testosterone levels are super high.

20 yo F has breasts and no uterus, karyotype reveals a 46 XX phenotype.

20 yo F has no breasts, but has a uterus, she can’t smell

20 yo F is 3’ 5” tall, low posterior hairline, widely spaced nipples, BP of 150/120 in the arms and a
BP of 65/40 in the legs, has a uterus, no breasts.

20 yo F with a uterus, no breasts, and visual field deficits.

Q11 Key Part 1
Match the clinical presentation of primary amenorrhea to the most likely
diagnosis;

20 yo F has breasts and a uterus, levels of all hormones are

normal-imperforate hymen, or anything weird that blocks the vagina. She is
actually menstruating, but the blood is not making its way out. Dx is by PE, tx
is with surgery.

20 yo F supermodel (or hardcore athlete) has breasts and a uterus (what

should be true of her hormone levels?)-this is either anorexia nervosa/just
working out too much. In the setting of severe physiologic stress, the GnRH
axis is turned off. Therefore, GnRH/LH/FSH/Estrogen levels are all low.
Q11 Key Part 2
Match the clinical presentation of primary amenorrhea to the most likely diagnosis;

20 yo F has breasts and no uterus, testosterone levels are super high-this is testicular feminization
syndrome (or Androgen Insensitivity Syndrome)-she has no uterus b/c she is 46 XY. Sertoli cells
make MIH so the mullerian duct is nuked (oviducts, uterus, upper third of the vagina). She has
breasts b/c the testosterone is aromatized to estrogen in the periphery. Why should she have an
orchiectomy after puberty?

20 yo F has breasts and no uterus, karyotype reveals a 46 XX phenotype-Mullerian Agenesis

(Mayer Rokitansky Kuster Hauser Syndrome). For whatever reason, the mullerian duct does not
develop so there’s no uterus. She has ovaries which produce estrogen (ovaries are not derived
from the mullerian ducts) so she has breasts. Whenever you see breasts, estrogens are around.
Whenever you see pubic hair, think androgen availability.

20 yo F has no breasts, but has a uterus, she can’t smell-Kallmann Syndrome, everything will be
low-GnRH down. No breasts b/c the ovaries are making no estrogen. Give pulsatile leuprolide.
Q11 Key Part 3
Match the clinical presentation of primary amenorrhea to the most likely diagnosis;

20 yo F is 3’ 5” tall, low posterior hairline, widely spaced nipples, BP of 150/120 in the arms and a
BP of 65/40 in the legs, has a uterus, no breasts-this is Turner’s syndrome. Don’t read too much
into the details here but you need to commit all of this to memory for Step 1. Turner’s is a kind of
hypergonadotropic hypogonadism (streak ovaries) so the FSH levels will be high. Karyotype is 45
XO. Common associations include bicuspid aortic valves, coarctation of the aorta (BP differences
b/w the arms and legs), horseshoe kidney, amongst other anomalies. With the ovaries basically
non-existent, there is no estrogen (or very little), so there is no breast development.

20 yo F with a uterus, no breasts, and visual field deficits-some kind of brain tumor (like a
craniopharyngioma, considering the VF deficits). A compressive lesion of the anterior pituitary
may hamper LH/FSH production so the ovaries are not stimulated (so there’s no estrogen = no
breasts).
The Primary Amenorrhea Algorithm
Q12
Match the clinical presentation to the most likely diagnosis;

23 yo F has had menses before, missed her last 3 periods, urine B-HCG is +ve.

23 yo F has had menses before, missed her last 3 periods, was diagnosed with
schizophrenia 3 mo ago.

23 yo F has had menses before, missed her last 3 periods, biopsy reveals lymphoid
follicles in the thyroid.

23 yo F has had menses before, missed her last 3 periods, has galactorrhea.

35 yo F has had menses before, BMI of 32, irregular menses for the past 5 years.
Q12 Key (Secondary Amenorrhea)
Match the clinical presentation to the most likely diagnosis;

23 yo F has had menses before, missed her last 3 periods, urine B-HCG is +ve-yay!,
she’s pregnant.

23 yo F has had menses before, missed her last 3 periods, was diagnosed with
schizophrenia 3 mo ago-dopamine antagonists, hyperprolactinemia.

23 yo F has had menses before, missed her last 3 periods, biopsy reveals lymphoid
follicles in the thyroid-Hashimoto’s, high TRH/TSH, hyperprolactinemia.

23 yo F has had menses before, missed her last 3 periods, has

galactorrhea-prolactinoma (tx with bromocriptine, cabergoline).

35 yo F has had menses before, BMI of 32, irregular menses for the past 5 years-PCOS.
Q13
Match the clinical presentation to the most likely diagnosis;

30 yo M has been trying to have a kid with his wife for the past 2 years. PE reveals
what appears to be a “bag of worms” sensation on palpation of the testicles.

A Med20 student is performing a newborn exam. PE reveals a fluctuant testicular mass

that transilluminates with a pen light.
Q13 Key
Match the clinical presentation to the most likely diagnosis;

30 yo M has been trying to have a kid with his wife for the past 2 years. PE reveals
what appears to be a “bag of worms” sensation on palpation of the testicles-varicocele,
pampiniform plexus is dilated, more common on the left since the left renal vein has a
more tortuous course (has to cross over to the right side of the body to drain into the
IVC. It is very HY to differentiate b/w testicular vein drainage on the left vs the right,
similar relationships exists for the ovaries and adrenal glands, step 1 favorite!).
Infertility arises b/c the varicocele increases testicular temperature which impairs
sperm production.

A Med20 student is performing a newborn exam. PE reveals a fluctuant testicular mass

that transilluminates with a pen light-hydrocele. Arises secondary to failed obliteration
of the tunica/processus vaginalis, resolves w/time, increased risk of inguinal hernias.
Q14
23 yo F presents with vaginal bleeding. She is 8 weeks pregnant. She decided to come
in this morning after passing what appeared to look like a cluster of grapes at home.
Serum B-HCG is 320, 000. Her uterine fundus is palpated at the umbilicus.

What is the next best step in the management of this patient?

What should be seen with the testing modality from the first question?

What is your diagnosis?

How is this condition treated?

What are the 2 types of this condition?

What is the underlying pathophysiology?

Q14 Key
23 yo F presents with vaginal bleeding. She is 8 weeks pregnant. She decided to come
in this morning after passing what appeared to look like a cluster of grapes at home.
Serum B-HCG is 320, 000. Her uterine fundus is palpated at the umbilicus

What is the next best step in the management of this patient?-Transvaginal Ultrasound
(TVUS). Consider molar pregnancy in an exam Q detailing a fundal height/uterine size
that is too high for the “real” gestational age/B-HCG that is astronomical.

What should be seen with the testing modality from the first question?-Snowstorm
appearance.

What is your diagnosis?-Gestational Trophoblastic Disease/Molar pregnancy.

How is this condition treated?-Suction Curettage.

Q14 Key contd.
What are the 2 types of this condition?-Incomplete (69 XYY) and Complete (46 YY)
molar pregnancies.

What is the underlying pathophysiology?

Complete-arises from 1 sperm fertilizing an egg with no genetic material. The male
chromosomes double. With no viable female chromosomes, there is no fetus.

Incomplete-arises from 2 sperm fertilizing 1 egg. There’ll be an actual fetus.

Tx is with suction curettage. The lady will have to be placed on OCPs for 1 year with
serial measurements of B-HCG. It should go to zero. A rise after treatment is indicative
of recurrence, new pregnancy (this possibility is almost entirely prevented by placing
the patient on OCPs), mets, or choriocarcinoma (which has B-HCG as a tumor
marker, consider getting a CXR if there’s concern).
Q15
A 15 yo M studying for his exam has the sudden onset of intense groin pain. He moans
for 30 mins until his parents decide to bring him to the ED. His vitals are stable. No
testicular response is observed when his thighs are stroked with a tongue depressor.

What is the next best step in the management of this patient?

What is your working diagnosis?

How should this patient be treated?

How can a similar episode be prevented in the future?

Q15 Key
A 15 yo M studying for his exam has the sudden onset of intense groin pain. He moans
for 30 mins until his parents decide to bring him to the ED. His vitals are stable. No
testicular response is observed when his thighs are stroked with a tongue depressor.

What is the next best step in the management of this patient?-Emergent surgical
consult although a testicular US with color flow doppler is not a bad idea if this will
not delay treatment. This patient has 4-6 hrs before his testicles stop working.

What is your working diagnosis?-Testicular torsion. Consider in the setting of acute

onset testicular pain, transverse lie on exam, and an absent cremasteric reflex.

How should this patient be treated?-Detorse the affected testicle. Orchiopexy for both
(affected/unaffected) OR orchiopexy (good testicle)/orchiectomy (dead testicle).

How can a similar episode be prevented in the future?-Orchiopexy.

Q16
Match the info cluster to the most likely diagnosis;

Female phenotype up until age 11.

Over a few months, begins to assume a male phenotype.

46 XY karyotype.

Has testes.
Q16 Key
Match the info cluster to the most likely diagnosis;

Female phenotype up until age 11.

Over a few months, begins to assume a male phenotype.

46 XY karyotype.

Has testes.

-5 Alpha Reductase deficiency. Testosterone helps with the development of internal

male sex organs. DHT is needed for virilization of external male sex organs. With a
5AR deficiency, DHT is not made, so external “virilization” does not occur. At puberty,
the super high levels of testosterone overrides this process and leads to virilization.
Make sure you know and understand this disorder!
Q17
Match the following info cluster to the most likely diagnosis;

6 ft tall male

Small penis

High FSH/LH

Gynecomastia

Infertility
Q17 Key
Match the following info cluster to the most likely diagnosis;

6 ft tall male

Small penis

High FSH/LH

Gynecomastia

Infertility

-Klinefelter’s Syndrome (47 XXY). Testes are nonfunctional. There’s no negative

feedback on LH/FSH release so their levels are elevated.
Q18
Match the clinical presentation to the most likely diagnosis of spontaneous abortion;

Vaginal bleeding, a closed cervical os, a viable fetus on US

Vaginal bleeding, a closed cervical os, a non-viable fetus on US

Vaginal bleeding, an open/dilated cervical os, an intact gestational sac on US

Vaginal bleeding, an open/dilated cervical os, some products of conception visible on US

Vaginal bleeding, an open/dilated cervical os, no products of conception visible on US

Q18 Key
Match the clinical presentation to the most likely diagnosis of spontaneous abortion;

Vaginal bleeding, a closed cervical os, a viable fetus on US-threatened abortion.

Vaginal bleeding, a closed cervical os, a non-viable fetus on US-fetal demise.

Vaginal bleeding, an open/dilated cervical os, an intact gestational sac on US-inevitable

abortion.

Vaginal bleeding, an open/dilated cervical os, some products of conception visible on

US-incomplete abortion.

Vaginal bleeding, an open/dilated cervical os, no products of conception visible on

US-complete abortion.
Spontaneous Abortion
-First trimester bleeding has many causes but one of the big things you should
consider for your exam is a spontaneous abortion.

-The MCC of a spontaneous abortion in the first trimester is a fetal aneuploidy

(commonly trisomy 16).

-The easiest way to remember the different permutations is to think of the different
kinds of spontaneous abortion as being on a continuum from;

Threatened-Missed-Inevitable-Incomplete-Complete.

-Quite sobering.
Q19
23 yo F presents with a sudden onset of left lower abdominal pain and vaginal
bleeding. Her UPT is +ve. TVUS reveals no fetal tissue.

What is the your diagnosis?

How can this condition be managed?

Assuming an asymptomatic presentation with a serum B-HCG measured initially on

presentation at 1000 mIU/ml, how would you approach this patient?

What is the most likely location of the patient’s underlying problem?

Q19 Key
23 yo F presents with a sudden onset of left lower abdominal pain and vaginal bleeding. Her UPT
is +ve. TVUS reveals no fetal tissue.

What is the your diagnosis?-Ectopic Pregnancy.

How can this condition be managed?-If unruptured (salpingostomy-remove fetus, keep the
fallopian tube), if ruptured or a huge ectopic (salpingectomy-remove fetus and tube), for low risk
ones, medical therapy with Methotrexate is an option (inhibits dihydrofolate reductase, give
leucovorin rescue with extensive BMS). For any approach, follow B-HCG levels after tx (just like
you would for molar pregnancies).

Assuming an asymptomatic presentation with a serum B-HCG measured initially on presentation

at 1000 mIU/ml, how would you approach this patient?-repeat the B-HCG in like 2 days, if it does
not rise by at least two thirds, you should be concerned. At a B-HCG of 1k, the fetus is invisible.

What is the most likely location of the patient’s underlying problem?-ampulla of fallopian tube.
Q20-Do You Want To A Pregnant Millionaire???
Match the pregnancy change to the most likely 1 liner;
A blue/purple cervix and vagina
Blotchy pigmentation of the face
Changes in arterial blood pressure (first 20 weeks)
Changes in arterial blood pressure (after 20 weeks)
Plasma volume changes
Systemic Vascular Resistance changes/Oncotic pressure changes
Cardiac output changes
Cardiac output changes with being supine
RBC mass changes
Hgb/Hct changes
Levels of coagulation factors
Gastric motility/gastric emptying time
Colonic motility/colonic transit time
Effects of gastric motility/colonic motility changes
Acid base imbalance/Tidal volume change
Ureteral size changes
Changes in serum BUN/Cr/GFR/Creatinine Clearance
Glucose and Protein levels in the urine
Pituitary size changes/possible sequelae of this change
Thyroid size change/TBG change/Thyroid hormone levels/Free thyroid hormone
B-HCG levels
Q20 Key-Do You Want To Be A Pregnant Millionaire???
Match the pregnancy change to the most likely 1 liner;
A blue/purple cervix and vagina-Chadwick’s sign (progesterone vasodilation increases vascularity).
Blotchy pigmentation of the face-Chloasma.
Changes in arterial blood pressure (first 20 weeks)-decrease (progesterone is a smooth muscle relaxant).
Changes in arterial blood pressure (after 20 weeks)-increase (but still ends up being less than normal).
Plasma volume changes-increases 50% (makes sense, mom loses blood during delivery, so she should prepare!)
Systemic Vascular Resistance changes/Oncotic pressure changes-decrease (progesterone)/decrease (low albumin).
Cardiac output changes-increase (HR and SV-from increased plasma volume-both go up).
Cardiac output changes with being supine-decrease (uterus compresses the IVC).
RBC mass changes-increase by 30% (O2 carrying capacity goes up).
Hgb/Hct changes-decrease (remember that Hct is a mass/volume ratio-plasma volume goes up more than RBC mass).
Levels of coagulation factors-increase (pregnancy is a hypercoagulable state).
Gastric motility/gastric emptying time-decrease/increase (predisposes to heartburn from reflux of gastric contents).
Colonic motility/colonic transit time-decrease/increase-again all from progesterone mediated smooth muscle relaxation
Effects of gastric motility/colonic motility changes-gastric reflux (heartburn)/constipation.
Acid base imbalance/Tidal volume change-respiratory alkalosis secondary to hyperventilation (TV increases).
Ureteral size changes-increase (from progesterone vasodilation), causes urinary stasis, increased UTI risk.
Changes in serum BUN/Cr/GFR/Creatinine Clearance-decrease/decrease/increase/increase.
Glucose and Protein levels in the urine-increase (glucose transport maximum goes down in the PCT).
Pituitary size changes/possible sequelae of this change-increase (producing more hormones)/Sheehan’s Syndrome.
Thyroid size change/TBG change/Thyroid hormone levels/Free thyroid hormone-first 3 increase/last is unchanged.
B-HCG levels-increase for first 10 weeks, then decrease, more HCG = more vomiting (hyperemesis gravidarum).
Diagnosing and Dating Pregnancy
-Pregnancy is diagnosed with a B-HCG which can often be detected in the serum up to
1 week before it can be detected in the urine.

-Checking the B-HCG will be the next best step in management for a host of
practice/real exam Q’s you’ll encounter ->woman presenting with amenorrhea, woman
presenting with concerning signs for an ectopic pregnancy, etc.

-A woman’s due date can be derived by adding 7 days to the first day of her LMP,
subtracting 3 mo, and adding 1 year (Naegele’s Rule).

-For example, a woman with the first day of her LMP being August 8 2017 will be due
on the 15th of May 2018 (add 7 days, August 15 2017; subtract 3 mo May 15 2017; Add 1
year May 15 2018).
Pituitary Apoplexy vs Sheehan Syndrome
-This occasionally presents as a bit of confusion for many students as there are some
similarities. However, there are certain things that should point you in the right
direction.

-Sheehan syndrome is an ISCHEMIC process. It involves the pituitary getting infarcted

from a hypoperfusive process. It almost always occurs in the setting of PREGNANCY
on exams since the pituitary grows really large and is hence more susceptible to
ischemia compared to the “ground state” pituitary. Classic presentation is as a failure
to lactate (why)?

-Pituitary Apoplexy is a HEMORRHAGIC process. It involves bleeding into the

pituitary, classically in the setting of a macroadenoma.

-Sheehan syndrome is to an ischemic stroke as pituitary apoplexy is to a hemorrhagic

stroke (like a subarachnoid hemorrhage).
Q21-Testicular Tumor Triggers
Most common germ cell tumor
Highly radiosensitive, fried egg appearance
As an aside, what is the brain tumor that has a fried egg appearance?
Most common testicular tumor in men > 60 yo
Testicular tumor in the setting of “male” precocious puberty
Tumor containing trophoblastic tissue
Histological finding with Leydig Cell Tumors
Seminoma counterpart in females
Testicular tumor most commonly associated with elevated AFP
Testicular tumor in the setting of low TSH levels
Testicular tumor associated with Schiller Duval bodies
Tumor marker for choriocarcinoma
Testicular tumor with tissue resembling glomeruli
Tumor marker that rules out a seminoma
Most common testicular tumor in children
Next best step in the management of a palpable testicular mass
Q21 Key-Testicular Tumor Triggers
Most common germ cell tumor-seminoma (most common testicular tumor)
Highly radiosensitive, fried egg appearance-seminoma.
As an aside, what is the brain tumor that has a fried egg appearance?-oligodendroglioma.
Most common testicular tumor in men > 60 yo-testicular lymphoma (mets to testes).
Testicular tumor in the setting of “male” precocious puberty-Leydig Cell Tumor.
Tumor containing trophoblastic tissue-choriocarcinoma, hematogenous spread (brain/lungs).
Histological finding with Leydig Cell Tumors-Reinke crystals.
Seminoma counterpart in females-Dysgerminoma.
Testicular tumor most commonly associated with elevated AFP-Endodermal sinus tumor.
Testicular tumor in the setting of low TSH levels-choriocarcinoma (HCG can cause hyperthyroid
symptoms since it has a similar alpha subunit to TSH, elevated T4 will suppress TSH release).
Testicular tumor associated with Schiller Duval bodies-Endodermal Sinus (yolk sac) tumors.
Tumor marker for choriocarcinoma-B-HCG.
Testicular tumor with tissue resembling glomeruli-Schiller Duval bodies (Endodermal Sinus).
Tumor marker that rules out a seminoma-AFP.
Most common testicular tumor in children-Endodermal Sinus (yolk sac tumor).
Next best step in the management of a palpable testicular mass-orchiectomy (do not biopsy
suspected testicular cancer, you’ll get sued for promoting recurrence!)
Q22
Match the clinical presentation to the most likely diagnosis;

32 yo multigravida presents with painless 3rd trimester bleeding. US reveals a fetus

lying in the transverse position. The placenta is attached at the lower segment of the
uterus.

32 yo multigravida has had a protracted course of labor, delivering a well appearing

fetus 2 hrs ago. She has continued to bleed profusely. US reveals;

Placental attachment to the edge of the myometrium

Placental invasion of the uterine serosa

Placental invasion of the myometrium

Q22 Key
Match the clinical presentation to the most likely diagnosis;

32 yo multigravida presents with painless 3rd trimester bleeding. US reveals a fetus lying in the
transverse position. The placenta is attached at the lower segment of the uterus-Placenta Previa.
The low implantation of the placenta subjects it to “stretching” forces that occur when the lower
part of the uterus expands in late pregnancy. This can cause severe bleeding and some really bad
consequences for mom and baby.

32 yo multigravida has had a protracted course of labor, delivering a well appearing fetus 2 hrs
ago. She has continued to bleed profusely. US reveals;

Placental attachment to the edge of the myometrium-placenta accreta.

Placental invasion of the uterine serosa-placenta percreta.

Placental invasion of the myometrium-placenta increta.

The Menstrual Cycle
The Mechanism Of The Menstrual Cycle
-Menses begin on average b/w the 12-13 age range in females. Delay is considered when
this process has not begun by 16.

-The average female goes through 360 reproductive cycles before hitting menopause
which signifies the end of reproductive potential.

-The endometrium has 2 layers-functionalis (closer to the lumen) which sloughs off in
the process of menstruation AND the basalis (which is always present and regenerates
the functionalis layer).

-Menstruation occurs from a fall in the levels of progesterone which leads to spiral
arteriolar spasm, necrosis, and the release of prostaglandins.

-There are 2 phases to the menstrual cycle. The first phase is the proliferative phase
which ranges from 7-21 days with an average of 14 days.
The Mechanism Of The Menstrual Cycle contd.
-The second phase is the secretory (or luteal phase) which comes after ovulation. This phase
appears to be dependent almost primarily on the lifespan of the corpus luteum.

-It is very HY to know that variations in the length of cycles arise from variations in the
length of the proliferative phase, not the length of the luteal phase.

-The entire process begins with the pulsatile release of GnRH from the hypothalamus which
progresses to FSH release from the anterior pituitary as highlighted on the next slide.

-The FSH stimulates follicle maturation and estrogen production. As estrogen levels rise,
FSH levels fall. The reduced FSH levels are still enough to promote maturation of the
dominant follicle b/c this follicle possesses more FSH receptors which makes it more
sensitive to reduced FSH levels.

-At some magic point, E2 actually exerts +ve feedback on the hypothalamus and the AP
which leads to an LH surge and subsequent ovulation.
The HPG axis and its role in menstruation
The Mechanism of The Menstrual Cycle contd.
-Prior to ovulation, the high levels of E2 promotes the development of a proliferative
type of endometrium. With ovulation, the corpus luteum begins to produce
progesterone. The elevated progesterone and depressed E2 promotes the development
of “secretory” endometrium which is more conducive to pregnancy.

-B-HCG which comes from an implanted placenta tells the corpus luteum to keep
making progesterone for 10 weeks which maintains the uterine lining until the
placenta can begin to make enough progesterone to maintain the lining itself.

-In the absence of fertilization/implantation, there is no B-HCG, the corpus luteum

dies, there’s no progesterone, and spiral arteriolar spasm and necrosis occurs which
leads to menstruation. This marks the beginning of the next menstrual cycle with the
process beginning all over again.

-The next slide details this process.

The HPG axis and its role in menstruation
A Summary Of The Menstrual Cycle
Q23
Match the clinical presentation to the most likely diagnosis;

35 yo primigravida presents at 26 weeks gestation for a prenatal evaluation. Her BP is

155/96 mmHg. On another visit at 27 weeks, her BP is 156/97 mmHg.

35 yo primigravida presents at 26 weeks gestation for a prenatal evaluation. Her BP is

measured to be 155/96. On another visit at 27 weeks, her BP is 157/98. A 24 hr urine
protein collection is measured at 1.2g.

32 yo primigravida presents at 8 weeks gestation for her first trimester visit. Her BP is
measured at 149/97. Another BP measured the following week is 152/98.
Q23 Key
Match the clinical presentation to the most likely diagnosis;

35 yo primigravida presents at 26 weeks gestation for a prenatal evaluation. Her BP is

155/96 mmHg. On another visit at 27 weeks, her BP is 156/97 mmHg-Gestational HTN
(dx must be made > 20 wks, in many cases, remits at 12 wks postpartum).

35 yo primigravida presents at 26 weeks gestation for a prenatal evaluation. Her BP is

measured to be 155/96. On another visit at 27 weeks, her BP is 157/98. A 24 hr urine
protein collection is measured at 1.2g-preeclampsia, BP > 140/90 WITH
PROTEINURIA.

32 yo primigravida presents at 8 weeks gestation for her first trimester visit. Her BP is
measured at 149/97. Another BP measured the following week is 152/98-chronic HTN.
Dx made prior to 20 weeks. DOCs include a-methyldopa, labetalol, and hydralazine.
For Step 1, remember drug induced lupus with hydralazine (anti-histone antibodies).
Q24
32 yo primigravida presents at 30 weeks gestation with shortness of breath. Her BP is
measured at 180/120.

What is the next best step in the management of this patient?

The patient begins to have generalized, violent motor contractions. What is the next
best step in the management of this patient? What is your new diagnosis.

Assuming this patient has a plt count of 45k, AST/ALT of 1000 with a CBC revealing a
reduced haptoglobin, elevated LDH, and indirect hyperbilirubinemia. What is your
new diagnosis?
Q24 Key
32 yo primigravida presents at 30 weeks gestation with shortness of breath. Her BP is
measured at 180/120.

What is the next best step in the management of this patient?-Administer

alpha-methyldopa, labetalol, or hydralazine. BP interventions often begin at > 160/110.

The patient begins to have generalized, violent motor contractions. What is the next
best step in the management of this patient? What is your new diagnosis-Administer
MgSO4. Deliver the baby ASAP!. This is eclampsia.

Assuming this patient has a plt count of 45k, AST/ALT of 1000 with a CBC revealing a
reduced haptoglobin, elevated LDH, and indirect hyperbilirubinemia. What is your
new diagnosis?-this is HELLP syndrome (Hemolysis, Elevated Liver Enzymes, Low
Platelets). From this Q, you can hopefully see how Step 1 can easily integrate heme
with repro. The Q will not be this straightforward.
Q25-18 yo F with sudden onset flank pain while studying
Q25 Key-18 yo F with sudden onset flank pain while studying
Consider ovarian torsion. HY association with females that
have anything that makes the ovaries “bulky” like a
cyst/neoplasm. Involves suspensory ligament twisting. Dx can
be made with ultrasound (with doppler). Detorse ASAP.
Q26
Match the info cluster to the most likely diagnosis.

-Pain with intercourse.

-Pain that gets worse as menses approach. “Peak pain” is at onset of menses.

-30 yo F that has been trying to get pregnant for years.

Q26 Key
Match the info cluster to the most likely diagnosis.

-Pain with intercourse.

-Pain that gets worse as menses approach. “Peak pain” is at onset of menses.

-30 yo F that has been trying to get pregnant for years.

-Endometriosis. Very HY cause of infertility, associated with the classic triad of

dysmenorrhea (painful menses), dyspareunia (pain with intercourse/penetration), and
infertility. Defined as the presence of endometrial glands in sites other than the uterus.
Please do not confuse with adenomyosis which is defined as the presence of
endometrial glands in the myometrium.
Q27-71 yo F with ascites and a pelvic mass. Specific Dx?
Q27 Key-71 yo F with ascites and a pelvic mass. Specific dx?

Ovarian serous cystadenocarcinoma. Most common malignant ovarian neoplasm. Note

the HY association with “psammoma bodies”.
Q28-71 yo F presents with adnexal mass, US reveals a thick endometrial stripe
Q28 Key-71 yo F presents with adnexal mass, US reveals a thick endometrial stripe

Granulosa cell tumor. Secretes estrogen. Consider in a postmenopausal female that

presents with bleeding/big uterus/adnexal mass. Note the Call-Exner bodies.
Q29-16 yo F presents with a large adnexal mass
Q29 Key-16 yo F presents with a large adnexal mass
Benign, mature cystic teratoma (called a dermoid cyst). Contains tissue from different
germ cell layers. Can be very large. Struma Ovarii may cause hyperthyroidism.
Q30
Match the info cluster to the most likely diagnosis.

-70 yo F presents with early satiety.

-Adnexal mass detected on PE.

-Massive GI ascites with associated hepatic lesions.

-Histology reveals signet ring cells.

Q30 Key
Match the info cluster to the most likely diagnosis.

-70 yo F presents with early satiety.

-Adnexal mass detected on PE.

-Massive GI ascites with associated hepatic lesions.

-Histology reveals signet ring cells.

-Krukenberg tumor. GI malignancy that metastasizes to the ovary. Remember the

classic association with signet ring cells. Very poor prognosis. For your test, you should
also associate signet ring cells with Lobular Carcinoma In Situ (LCIS) which is
associated with an increased risk of bilateral breast cancer and E-Cadherin mutations.
Q31
Match the clinical presentation to the most likely diagnosis;

35 yo F presents with a 6 mo history of painful intercourse. Pelvic exam reveals

involuntary contractions of the perineal muscles. Sexual desire is normal. She is the VP
at a hedge fund.

35 yo F presents with a 6 mo history of painful intercourse. PE is completely normal.

Light touch of the perineal area reveals intense pain.
Q31 Key
Match the clinical presentation to the most likely diagnosis;

35 yo F presents with a 6 mo history of painful intercourse. Pelvic exam reveals

involuntary contractions of the perineal muscles. Sexual desire is normal. She is the VP
at a hedge fund-vaginismus (genito pelvic pain disorder, penetration disorder). The Q
stem contains the key pieces of information you’ll most likely be tested on.

35 yo F presents with a 6 mo history of painful intercourse. PE is completely normal.

Light touch of the perineal area reveals intense pain-vulvodynia. These patients have
an increased sensitivity to any kind of touch in the vulva/vaginal area. Associated with
long standing OCP use.
Q32
Match the clinical description to the most likely diagnosis;

33 yo F presents with a bloody nipple discharge.

23 yo F with an uneventful delivery 3 weeks ago presents with unilateral breast

swelling and erythema. Some purulent discharge is expressed on palpation of the
affected breast. Her body temperature is 103.

22 yo F presents with bilateral breast pain. PE reveals “lumpy-bumpy” breasts

bilaterally. A biopsy of one of the lesions reveals what appears to be a “blue domed
cyst”. Is the most common cause of a painful breast mass in the US.
Q32 Key
Match the clinical description to the most likely diagnosis;

33 yo F presents with a bloody nipple discharge-intraductal papilloma. Very HY to know

this for your test and for many exams in the future (even in M3/4).

23 yo F with an uneventful delivery 3 weeks ago presents with unilateral breast swelling and
erythema. Some purulent discharge is expressed on palpation of the affected breast. Her
body temperature is 103-this is mastitis (-> abscess). Very common in breastfeeding women.
Usually S. Aureus from cracks in the nipple. Give dicloxacillin.

22 yo F presents with bilateral breast pain. PE reveals “lumpy-bumpy” breasts bilaterally. A

biopsy of one of the lesions reveals what appears to be a “blue domed cyst”. Is the most
common cause of a painful breast mass in the US-fibrocystic change. Classically looks like a
bunch of weird animals on histology. Mostly benign. There’s cysts (clear spaces) with
fibrosis around the cysts (hence the name).
Some Other Breast Considerations
-It is also HY to know that breastfeeding is associated with a decreased risk of;

Breast cancer-Prolactin shuts down GnRH which nukes estrogen production. Estrogen
drives many breast cancers.

Ovarian cancer-Prolactin shuts down GnRH which causes anovulation. With

anovulation, the ovarian epithelium does not have to be broken down and repaired
each month (which happens with ovulation). This reduces the potential for malignant
transformation of ovarian epithelium.

-Breast feeding also helps with weight loss.

-A woman with HIV, active TB, or active herpes lesions on the breast should not
breastfeed. Should a woman with mastitis (S. Aureus, give dicloxacillin) breastfeed?
Galactosemia is also a contraindication to breastfeeding.
Fibrocystic Change
Q33
Match the clinical description to the most likely diagnosis;

41 yo F presents with a palpable breast mass. Mammogram reveals a focus of

calcification in the upper outer quadrant of her left breast. Histology reveals lipid laden
mononuclear cells. She was recently punched in the left breast by a loser.

23 yo F presents with a painless, discrete, movable breast mass. She is 25 weeks

pregnant by her LMP. She noticed the mass at 6 weeks gestation. The mass has grown
significantly since it was first noticed.

The 4 most common gynecologic cancers in the US (by incidence and by number of
deaths).
Q33 Key
Match the clinical description to the most likely diagnosis;

41 yo F presents with a palpable breast mass. Mammogram reveals a focus of calcification in the
upper outer quadrant of her left breast. Histology reveals lipid laden mononuclear cells. She was
recently punched in the left breast by a loser-this is fat necrosis. The history seals the deal.

23 yo F presents with a painless, discrete, movable breast mass. She is 25 weeks pregnant by her
LMP. She noticed the mass at 6 weeks gestation. The mass has grown significantly since it was
first noticed-fibroadenoma. Most common benign breast mass in women < 35. Is a tumor of the
fibrous breast stroma, hence the term. Is E2 sensitive and can increase in size with pregnancy/the
menstrual cycle.

The 4 most common gynecologic cancers in the US (by incidence and by number of deaths)-by
incidence (breast, endometrial, ovarian, cervical). By deaths (breast, ovarian, endometrial,
cervical).
Q34
A 53 yo postmenopausal female presents with a palpable breast mass. The mass has been present
for the last 6 months and has not changed in size. PE reveals a fixed mass.

What are the genetic syndromes associated with the most likely diagnosis?

What does the age at menarche/menopause have to do with the most likely diagnosis?

If PE reveals a firm, nontender, irregular mass with redness, skin dimpling, a “peau d’orange
appearance”, and nipple retraction, what would your diagnosis be?

What is the most common kind of breast cancer?

An excisional biopsy reveals neoplastic cells with IHC indicating ER and PR positivity. What is
the next best step in pharmacological treatment?

What should you consider in the setting of eczematous nipple changes in a 70 yo F?

Q34 Key
A 53 yo postmenopausal female presents with a palpable breast mass. The mass has been present for the last 6
months and has not changed in size. PE reveals a fixed mass.

What are the genetic syndromes associated with the most likely diagnosis-BRCA 1 and 2. HNPCC, Li-Fraumeni
syndrome (p53 mutations)

What does the age at menarche/menopause have to do with the most likely diagnosis-being young at menarche,
older at menopause increases E2 exposure which can increase breast cancer risk.

If PE reveals a firm, nontender, irregular mass with redness, skin dimpling, a “peau d’orange appearance”, and
nipple retraction, what would your diagnosis be-inflammatory BC with mets to subdermal lymphatics.

What is the most common kind of breast cancer-infiltrating ductal carcinoma.

An excisional biopsy reveals neoplastic cells with IHC indicating ER and PR positivity. What is the next best
step in pharmacological treatment-tamoxifen (SERM), anastrozole (aromatase inhibitor).

What should you consider in the setting of eczematous nipple changes in a 70 yo F-Paget’s disease.
Breast Cancer
-Screening often done with yearly mammograms after 40.

-Most breast cancers metastasize to axillary nodes. Some to internal mammaries.

-Infiltrating lobular cancer is associated with E-Cadherin mutations (cells do not

adhere to each other) and bilateral breast cancer. Consider in an exam Q detailing
cancer cells that stay in a “single file” on histology.

-Mets are often to lung, liver, brain, and bone (blastic lesions, lytics possible too).

-For cancers with the ERB2 mutation (bad prognosis), trastuzumab is an option (for
Step 1, remember reversible dilated cardiomyopathy vs non-reversible for the
anthracyclines which is prevented with dexrazoxane).

-For Step 1, the long thoracic nerve may be injured in breast surgery (winged scapula).
Benign Breast Lesions
Malignant Breast Lesions
Types of Breast Cancer
Quick Hits On Ovarian Cancers
Mucinous (Left), Brenner (Middle), Serous (Right)
Q35-Contraceptive Triggers
Match the clinical description to the most likely contraceptive;
Lasts 10 years
Inflammatory reaction in the uterus
Thickens cervical mucus
Most effective contraception mechanism
Permanent contraception applying to males
Permanent contraception applying to females
For the (2) above, which is more easily reversed?
2 least effective methods of contraception
Contraception that provides STI protection
Spermicides increase susceptibility to?
Lifestyle factor that is a combined OCP contraindication
Primary MOA of OCPs
2 cancers with lower incidence in the setting of OCP use
Irregular bleeding, weight gain, long time before fertility returns, depression
3 yr protection, progestin, no impact on weight/mood/bone
Q35 Key-Contraceptive Triggers
Match the clinical description to the most likely contraceptive;
Lasts 10 years-Paragard (Cu IUD vs Mirena which is for 5 yrs in the US and 7 yrs in Europe).
Inflammatory reaction in the uterus-Paragard.
Thickens cervical mucus-Progestins (like the Mirena).
Most effective contraception mechanism-abstinence.
Permanent contraception applying to males-Vasectomy.
Permanent contraception applying to females-Tubal ligation.
For the (2) above, which is more easily reversed-vasectomy.
2 least effective methods of contraception-natural family planning, “pull out methods”.
Contraception that provides STI protection-condoms.
Spermicides increase susceptibility to-HIV infection (inflammation nukes vaginal mucosa).
Lifestyle factor that is a combined OCP contraindication-smoking (also hx of DVT, strokes, etc).
Primary MOA of OCPs-shut off the HPG axis.
2 cancers with lower incidence in the setting of OCP use-endometrial and ovarian.
Irregular bleeding, weight gain, long time before fertility returns, depression-Depo-Provera (3 mo
shot).
3 yr protection, progestin, no impact on weight/mood/bone-Nexplanon (progesterone implant).
Contraception->Key Takeaways 1
-The only contraceptive methods that protect against STDs are abstinence/condoms.

-Combined OCPs work by inhibiting ovulation (E2 -ve feedback) and increasing the
thickness of cervical mucus (progesterone).

-Avoid combined OCPs in individuals with a history of a DVT/PE/Weird genetic

diseases like Factor 5 Leiden. You should avoid these agents in individuals with a
history of cancers driven by E2 (like breast), people with bad HTN, patients with
hepatic adenomas, and smokers > 35 yo. Another unusual contraindication is in a
patient who has a h/o migraine with aura/atypical migraine involving neuro deficits.

-Combined OCPs decrease the risk of ovarian/endometrial cancer (fewer cycles).

-If a lady is being treated for TB and becomes pregnant with regular combined OCP
use, think of revved up metabolism from rifampin mediated CYP450 induction.
Contraception->Key Takeaways 2
-Progestin only pills have the MOA that involves thickening cervical mucus. Do not
forget the associations with weight gain and reversible osteoporosis. These are good
postpartum options.

-A progesterone derivative (Megestrol) is given to stimulate the appetite in cachectic

patients.

-The Cu IUD is an excellent contraceptive that works by causing an inflammatory

reaction that makes the uterus inhospitable for sperm and eggs. Avoid this option is a
woman has a history of heavy menses. An unusual association is the contraindication
of this contraceptive method in patients with Wilson’s disease.

-Remember the association of ectopic pregnancies with a history of tubal ligation.

Q36
Given the following clinical scenarios, what is the most likely diagnosis?

22 yo F is tearful 3 days after delivery. She has been breastfeeding and taking good care
of the baby.

22 yo F is brought to the ED by her husband 3 days after delivery. He found a small

radio taped to her head. She claims to be receiving detailed instructions from outer
space on how sacrificing her baby would end world hunger.

22 yo F comes to her 1 week postpartum visit. She looks dishevelled and admits to
occasionally having thoughts of hurting the baby which she feels remorseful about. She
has been breastfeeding the baby but no longer enjoys activities she loved before she
got pregnant. She is accompanied by her husband who appears to be supportive.
Q36 Key
Given the following clinical scenarios, what is the most likely diagnosis?

22 yo F is tearful 3 days after delivery. She has been breastfeeding and taking good care of the
baby-Postpartum blues. Reassure the parent, avoid prescribing medications.

22 yo F is brought to the ED by her husband 3 days after delivery. He found a small radio taped to
her head. She claims to be receiving detailed instructions from outer space on how sacrificing her
baby would end world hunger-Postpartum psychosis (consider with hallucinations, hearing
voices, etc). Hospitalize involuntarily if need be, start an atypical/typical antipsychotic.

22 yo F comes to her 1 week postpartum visit. She looks dishevelled and admits to occasionally
having thoughts of hurting the baby which she feels remorseful about. She has been breastfeeding
the baby but no longer enjoys activities she loved before she got pregnant. She is accompanied by
her husband who appears to be supportive-Postpartum depression. The patient will match 5/9 of
the SIGECAPS symptoms (including depressed mood or anhedonia) on your test. Don’t be
swayed by the presence of only 4 symptoms. Prescribe an SSRI.
Q37
A 15 yo F presents to the ED for severe abdominal pain and cramping. A physical exam
is notable only for suprapubic tenderness to palpation. Further questioning reveals that
the patient started having her period 3 months ago and has been having cycles for the
past 3 days. There is dried blood at the vaginal introitus. A serum B-HCG is negative
and the patient reports that she has never been sexually active. Her labs and vital signs
are within normal limits. What is the next best step in the management of this patient?

a. Administration of a cyclooxygenase inhibitor

b. Exploratory laparotomy
c. Broad spectrum antibiotic therapy
d. Sertraline therapy for depressive symptoms
Q37 Key
A 15 yo F presents to the ED for severe abdominal pain and cramping. A physical exam
is notable only for suprapubic tenderness to palpation. Further questioning reveals that
the patient started having her period 3 months ago and has been having cycles for the
past 3 days. There is dried blood at the vaginal introitus. A serum B-HCG is negative
and the patient reports that she has never been sexually active. Her labs and vital signs
are within normal limits. What is the next best step in the management of this patient?

a. Administration of a cyclooxygenase inhibitor

b. Exploratory laparotomy
c. Broad spectrum antibiotic therapy
d. Sertraline therapy for depressive symptoms

This patient most likely has primary dysmenorrhea (painful menses) which can be
treated with NSAIDS. Combined OCPs may be a good second option.
Q38
Given the following clinical descriptors, what is the most likely
diagnosis?

A 32 yo F presents to her PCP complaining of painful periods,

pain with sex, and painful bowel movements. She has been trying
to have kids since she got married 2 years ago. A pelvic exam
reveals a 6 cm tender mass in the rectouterine pouch (RUP)
along with nodularity of the uterosacral ligaments.
Q38 Key-Endometriosis
Given the following clinical descriptors, what is the most likely diagnosis?

A 32 yo F presents to her PCP complaining of painful periods, pain with sex, and
painful bowel movements. She has been trying to have kids since she got married 2
years ago. A pelvic exam reveals a 6 cm tender mass in the rectouterine pouch (RUP)
along with nodularity of the uterosacral ligaments.

This is endometriosis (deposition of endometrial tissue outside the uterus). There are
many theories as to why this occurs but “retrograde menstruation” is a commonly
peddled one. Consider this as your dx with mention of the 3D’s->dyschezia,
dysmenorrhea, and dyspareunia. The most common location is the ovary (where it can
bleed and cause an endometrioma) followed by the RUP. Definitive dx is with
laparoscopy. Tx options include combined/progestin OCPs (nuke HPG axis),
continuous GnRH (not pulsatile), and surgery if fertility is desired (or TAHBSO if
postmenopausal and reproduction is no longer required).
Q39
Given the following clinical descriptors, what is the most likely diagnosis?

A 40 yo F complains of increasing pain with menses for the past 11 months. Her
periods are extremely heavy. Her last child was delivered 12 years ago with a
subsequent tubal ligation. On pelvic exam, her uterus appears enlarged and tender
with a globular, soft consistency.
Q39 Key-Adenomyosis
Given the following clinical descriptors, what is the most likely diagnosis?

A 40 yo F complains of increasing pain with menses for the past 11 months. Her
periods are extremely heavy. Her last child was delivered 12 years ago with a
subsequent tubal ligation. On pelvic exam, her uterus appears enlarged and tender
with a globular, soft consistency.

This patient has adenomyosis (the deposition of endometrial glands in the

myometrium). In contrast with leiomyomas that are asymmetric, firm, and nontender
adenomyosis has a symmetric, soft, and tender uterine presentation. Dx is usually
clinical although an MRI may be helpful. The dx can only be made conclusively by the
examination of tissue after surgery. Tx is usually with the levonorgestrel IUD which
may curb the menstrual bleeding. Definitive treatment revolves around getting a
hysterectomy.
Q40
A 43 yo F schedules an appointment with her gynecologist 3 months after her annual
checkup. She has felt irritable and moody for the past 9 weeks and often has to change
out of her nightgown as a result of severe night sweats. Physical exam is notable for
mild pretibial edema. Vitals are notable for mild tachypnea. The patient is in a good
relationship with her husband of 20 years. She has regular, 30 day menstrual cycles
although she has recorded no flow for the past 2 cycles. What is the next best step in
the management of this patient?

a. Measure serum TSH levels

b. Check FSH and estrogen levels to rule out menopause
c. Endometrial sampling and biopsy to rule out an endometrial malignancy
d. Reassurance as this is normal
e. Measurement of serum B-HCG levels
Q40 Key
-The best answer here is E. This lady may be pregnant.

-As a rule (with very few exceptions), a reproductive age female

with amenorrhea deserves a pregnancy test.

-Don’t get dinged by questions that may try to make you think of
hypothyroidism or menopause first before ruling out pregnancy.

-Watch out for these kinds of scenarios on your test.

Q41-What is the most likely bug?
Chorioretinitis, hydrocephalus, intracranial calcifications, cat litter, give
pyrimethamine/sulfadiazine
Slapped cheek rash, arthritis in adults, anemia +/- fetal hydrops
Fetus born with scarred skin, hypoplastic limbs, life threatening PNA in fetus, mom had a
generalized rash during pregnancy with vesicles and blisters in different stages of healing
Mom consumed deli meats, stillborn fetus, abscesses in the heart, liver, spleen, give
ampicillin
Cataracts, deafness, machine like murmur in the newborn, blueberry muffin rash
Periventricular calcifications in the fetus, sensorineural HL/jaundice/HSM in fetus
Prevent infection by a scheduled C-Section, give AZT intrapartum during delivery
Give acyclovir ppx starting at 36 weeks w/hx of infection, deliver vaginally if there are no
“visible” lesions, deliver by C-Section if there are visible lesions
Sloughed skin of the hands and feets, tons of nasal secretions in the neonate, later in life the
kid has a prominent forehead, collapsed nasal bridge, Hutchinson's teeth, anterior tibial
bowing
Cause of meningitis, pneumonia, sepsis in the first 28 days of life
Q41 Key-What is the most likely bug?
Chorioretinitis, hydrocephalus, intracranial calcifications, cat litter, give pyrimethamine/sulfadiazine-T.Gondii
Slapped cheek rash, arthritis in adults, anemia +/- fetal hydrops-Parvovirus B19
Fetus born with scarred skin, hypoplastic limbs, life threatening PNA in fetus, mom had a generalized rash
during pregnancy with vesicles and blisters in different stages of healing-VZV (if mom is exposed during
pregnancy and unvaccinated, give VZIG. Don’t give the vaccine in pregnancy. If the neonate is exposed, give
VZIG as well. Give mom acyclovir if she is infected during pregnancy)
Mom consumed deli meats, stillborn fetus, abscesses in the heart, liver, spleen, give ampicillin-Listeria
Cataracts, deafness, machine like murmur in the newborn, blueberry muffin rash-rubella (don’t give vaccine in
pregnancy!)
Periventricular calcifications in the fetus, sensorineural HL/jaundice/HSM in fetus-CMV (ganciclovir)
Prevent infection by a scheduled C-Section, give AZT intrapartum during delivery-HIV (place mom on HAART
therapy that does not include efavirenz, for potential neonatal exposure, give 6 weeks of AZT prophylactically
and then do PCR testing at some point in the future)
Give acyclovir ppx starting at 36 weeks w/hx of infection, deliver vaginally if there are no “visible” lesions,
deliver by C-Section if there are visible lesions-HSV
Sloughed skin of the hands and feet, tons of nasal secretions in the neonate, later in life the kid has a prominent
forehead, collapsed nasal bridge, Hutchinson's teeth, anterior tibial bowing-Syphilis (RPR/VDRL for screening,
MHA-TP/FTA-ABS for confirmation, give Penicillin)
Cause of meningitis, pneumonia, sepsis in the first 28 days of life-S. Agalactiae/GBS
Endometrial Cancer
-Endometrial cancer (often adenocarcinoma) arises in the setting of endometrial
hyperplasia. The big RF is exposure to unopposed E2 (PCOS, obesity->from increased
amounts of aromatase, prolonged exposure to tamoxifen). There is also an association
with HNPCC.

-There are 2 types. Type 1 is the “classic” one associated with increased E2 exposure.
Type 2 is not associated with increased E2 exposure and has a horrible prognosis (it’s
like ovarian cancer in a sense).

-The classic presentation is abnormal uterine bleeding in a postmenopausal female.

Perform an endometrial biopsy. A HY scenario to be aware of is making sure you
perform an EMB in a female with a long hx of PCOS even if she is in her 30s
(especially if she presents with abnormal uterine bleeding).

-Treatment is with a TAHBSO. Prognosis is excellent if caught early.

Cervical Cancer
-Squamous cell cancer (outer cervix) is the most common kind of cervical cancer.
Adenocarcinomas can also occur but are typically in the inner cervix that is not
necessarily visible with a speculum exam.

-Most cancers arise in the transformation zone between the ecto and endocervix.

-The biggest RF is a history of exposure to HPV (especially 16 and 18). Other RFs
include having multiple sex partners, having a h/o of STDs, and having HIV
(immunosuppression). Smoking is also a RF.

-A woman should be screened every 3 years from 21-29. A similar regimen can be
pursued after the age of 30. However, a pap smear + HPV screening can be conducted
every 5 years. Screening can be stopped at 65 if multiple pap smears have been normal.
Cervical Cancer contd.
-Consider cervical cancer if a Q stem gives you a patient with the RFs discussed earlier
in the setting of post-coital bleeding.

-Cervical cancer can metastasize to structures of the urinary system (like ureters) and
cause hydronephrosis leading to renal failure. This is the MCCOD in cervical cancer.

-Remember the complication of cervical insufficiency (painless pregnancy loss) with

LEEP and conization procedures.
Q42
Given the following info cluster, what is the most likely diagnosis?

-Hypoplastic fetal lungs.

-Amniotic fluid index of 2 cm (oligohydramnios)

-Facial, skin, and limb defects.

Q42 Key
Given the following info cluster, what is the most likely diagnosis?

-Hypoplastic fetal lungs (usual cause of death)

-Amniotic fluid index of 2 cm (oligohydramnios)

-Facial, skin, and limb defects

This is Potter Syndrome which arises secondary to bilateral renal agenesis ultimately
leading to oligohydramnios and the many characteristic findings. Another HY cause of
oligohydramnios are posterior urethral valves.

On the flip side, consider polyhydramnios given a hx of anencephaly (no swallowing

center), maternal DM (hyperglycemia induced polyuria in the fetus), duodenal atresia
(double bubble sign), and esophageal atresia (an NGT is curled up in the upper
thoracic cavity).
Q43
A 15 yo primigravida presents to her PCP with complaints of severe morning sickness
and vaginal bleeding. She has been vomiting for hours everyday and has lost over 15
pounds since her LMP 8 weeks ago. She has been taking Benadryl to help with the
nausea. BP is 140/98, HR 103 bpm, RR 18 bpm. A transvaginal US reveals a central
heterogeneous mass in the uterus having a solid, hyperechoic area interspersed with a
multitude of cystic areas. B-HCG is positive. What is the next best step in the
management of this patient?

a. Recommendation for small, regular meal sizes.

b. Suction curettage.
c. Ondansetron therapy.
d. Immediate cesarean delivery.
e. Total abdominal hysterectomy with bilateral salpingo-oophorectomy.
Q43 Key
-The best answer here is B, suction curettage. This patient has a hydatidiform
mole.

-Risk factors include a prior hx of hydatidiform moles and being super

young/super old as a pregnant female.

-These moles arise from trophoblastic contents and are of 2 kinds->complete

and partial moles.

-Partial moles arise from the fertilization of one egg by 2 sperm which gives
rise to a triploid embryo (69 XXX/XXY/XYY). Partial moles contain fetal
tissue, produce increased amounts of HCG, have a small risk of progressing to
invasive moles, and essentially never progress to choriocarcinoma.
Q43 Key contd.
-Complete moles on the other hand are a lot worse. They arise from the fertilization of
an empty egg by 2 sperm OR from the fertilization of an empty egg by 1 sperm with
subsequent duplication of the genetic material (so there are 46 chromosomes).
Complete moles have no fetal tissue, produce tons of HCG, and have huge risks of
progression to invasive moles AND choriocarcinoma.

-Molar pregnancies may also present with a size of the uterus > dates or as
hyperemesis gravidarum.

-In the period following suction curettage for a molar pregnancy, the patient should be
on birth control for about 6 mo with the HCG values followed to zero as a means of
following disease recurrence/progression to the worrisome choriocarcinoma.
Q44
A 31 yo F presents to L&D at 37 weeks gestation with consistent, moderately painful
uterine contractions. Her pregnancy has been complicated by her history of diabetes
mellitus. Fetal heart tracings are unremarkable. The patient was offered a C-Section
secondary to fetal macrosomia but insisted on having a “natural” birth. During the
second stage of labor, the baby’s anterior shoulder is stuck under the pubic symphysis.
The baby is successfully delivered after repeated traction on the shoulder and arm in
addition to applying maneuvers involving hip flexion in the mom. This baby’s delivery
increases his risk of injury to?

a. The C5-6 roots of the brachial plexus

b. The C8-T1 roots of the brachial plexus
c. The C3-5 roots of the brachial plexus
d. The C5 and T1 roots of the brachial plexus
Q44 Key
-The best answer here is A. This baby has shoulder dystocia. Repeated traction on the
shoulder increases the risk of Erb Duchenne Palsy which is a lesion of the C5-6 roots
or upper trunk of the brachial plexus. Remember the classic description of the waiter’s
tip deformity (elbow extended, forearm pronated, MCPs flexed).

-In general, a baby on the larger side (usually > 4500g) should get a planned C-Section
since the risk of cephalopelvic disproportion is too high.
Postpartum Hemorrhage (Part 1)

According to ACOG. Blood loss;

-Greater than 500 ml after a vaginal
delivery.
-Greater than 1000 ml after a cesarean
section.
Uterine Atony (most common cause!)
Postpartum Hemorrhage (Other causes/summary)
Q45
A 21 yo F presents to her PCP with complaints of severe facial acne. Her LMP was 1
week ago. The patient is in a stable relationship with her boyfriend of 3 months and
they use condoms inconsistently. Physical exam is notable for open and closed
comedones clustered around the patient’s lower face. Prior attempts with tetracycline,
benzoyl peroxide, and combined OCPs have failed to yield any positive results. The
patient smokes 2 cigarettes per day and requests a prescription for isotretinoin. The
most likely contraindication to this treatment regimen is?

a. The patient’s age.

b. The patient’s history of smoking.
c. The patient’s history of unprotected sexual intercourse.
d. The patient’s history of pseudotumor cerebri.
e. There are no contraindications to the use of isotretinoin in this patient
population.
Q45 Key
-The best answer here is C, a history of unprotected sexual intercourse. Isotretinoin is a
potent teratogen and patients typically have to be on 2 forms of birth control to be on
this medication.

-Smoking is a contraindication to the use of combined OCPs but not isotretinoin.

-In addition to the teratogens listed 2 slides ago, remember the association between
AEDs and NTDs and thalidomide with limb anomalies (phocomelia).

- As an aside, cocaine use during pregnancy is associated with painful vaginal bleeding
in the 3rd trimester (abruption). A Q stem detailing a jittery, inconsolable newborn in
a mom with “dangerous habits” should clue you into withdrawal from some kind of
drug (more than likely opioids).
Q46
Given the following birth defects, what is the most likely teratogen?

RV hypoplasia, downward displacement of the tricuspid valve

Tooth discoloration
Cartilage damage
Stippling of the epiphyses, do not use this anticoagulant in a pregnant female
with a DVT
Clear cell adenocarcinoma of the vagina
Renal problems in the fetus
Gray Baby Syndrome
Kernicterus (buildup of toxic bilirubin metabolites in the brain)
Smooth philtrum, microcephaly, thin upper lip
IUGR, hypoplastic nails, microcephaly, cleft lip
Q46 Key
Given the following birth defects, what is the most likely teratogen?

RV hypoplasia, downward displacement of the tricuspid valve-Ebstein’s anomaly, Li

toxicity.
Tooth discoloration-Tetracycline (binds Ca, avoid in pregnant women/kids < 8).
Cartilage damage-Fluoroquinolones.
Stippling of the epiphyses, do not use this anticoagulant in a pregnant female with a
DVT-Warfarin (remember pregnancy is a hypercoagulable state w/Virchow’s triad, use
heparin instead, also HY to know that heparin is used for APLA syndrome). These women
should probably avoid E2 contraceptives in the future.
Clear cell adenocarcinoma of the vagina-Diethylstilbestrol (DES, also T shaped uterus).
Renal problems in the fetus-ACE-I and ARBs.
Gray Baby Syndrome-Chloramphenicol.
Kernicterus (buildup of toxic bilirubin metabolites in the brain)-TMP-SMX.
Smooth philtrum, microcephaly, thin upper lip-fetal alcohol syndrome.
IUGR, hypoplastic nails, microcephaly, cleft lip-Phenytoin (fetal hydantoin syndrome).
All The Best!