Professional Documents
Culture Documents
Oocytes
Spermatocytes
Genesis
Fetal life
Begins at puberty
Population
Max at birth, number drops with time
Production continues throughout life
Female
Target
Female
Product
Male
Target
Male
Product
LH
Theca Cells
FSH
Granulosa Cells
Androgenic precursors
(from cholesterol)
Leydig cells
Testosterone
Phase
Follicular Phase
Ovulation
Luteal Phase
Prominent Hormones
Estrogen
LH surge + FSH peak
Progesterone
Result
Endometrial proliferation
Follicle ruptures
Secretory endometrium
Menses
Withdrawal of progesterone
Shedding of endometrium
Feedback shut down during childhood because higher level NTs shut down GnRH (FSH > LH)
Prepubertal DESUPPRESSION of GnRH occurs gradually and first occurs during sleep (result = LH > FSH)
2.
Compare/contrast standards regarding timing of pubertal onset for girls and definition of precocious
puberty. (dont need to know numbers, just general)
Females
Males
First sign of
Thelarche (or adrenarche)
Testicular enlargement
puberty
Age
9-11
10-13.5
Subsequent
Growth spurt
Adrenarche (>10yrs)
events
Menarche (12.8 yrs)
Penile and prostatic enlargement (11-14 yrs)
Ovulation (<50% 1st yr,
Growth spurt
95% after 7 yrs; earlier if menarche is earlier)
Spermarche (EARLY 13.4 yrs)
Skeletal maturation (10.5-16 yrs)
Early puberty
Breast and/or pubic hair development
Very rare
Before age 6 (Af. American) or 7 (Caucasians)
Usually truly pathologic
10x more common than males, usually idiopathic
3.
Recite the differences between central (true) precocious puberty and peripheral (incomplete) precocious
puberty.
4. Give examples of causes of central and peripheral causes of precocious puberty in males and females and
their mechanisms.
Central (True)
Peripheral (Incomplete)
Definition
Acting through or at CNS -> complete pubertal
Appearance of one phase of puberty only
development
Gonadotro
Gonadotropin dependent
Gonadotropin Independent
pins
Cause
Early activation of arcuate nucleus with GnRH
Varies
secretion
LH/FSH
LH > FSH
Gender
Females > males
Males = isolated sexual development (androgens)
Females = isolated thelarche, adrenarche, or
menarche
GnRH?
Responsive (-> downregulation)
Unresponsive
Causes
Idiopathic (50-75%)
Thelarche:
Identified central causes: CNS lesions
Isolated precocious thelarche: after birth from
(hamartoma, neurofibroma, glioma, astrocytoma),
GnRH, will go away with childhood GnRH
hydrocephalus, encephalitis, vascular
suppression
malformation
McCune-Albright Syndrome: caf-au-lait spots,
Primary severe hypothyroidism (rare)
polyostic fibrous dysplasia; progressive, GnRH
independent; from GPCR G mt
Autonomous estrogen producing follicular cyst:
also GnRH independent
Adrenarche:
Isolated precocious adrenarche: likely normal,
adrenal origin
CAH: most commonly 21-OHase deficiency
Insulin resistance: harbinger of PCOS
Isolated Sexual Development:
Exogenous hormones: rare
Serious tumors: worry about these!
Thelarche
Tanner
I
Tanner
II
Tanner
III
Tanner
IV
Nothing
Breast budding
Tanner
V
Feature
s
Male genitalia
Enlargement of testes, penis, and
prostate
Preadolescent
1
Genetic
Sex
2
Formati
on
of Gonad
3
Formati
on of
Ductal
System
4
Differen
tiation
of
External
Genitali
a
Male
Female
Overview SRY (Sex-determining
After germ cell migration, only
region of Y) on short arm
requirement is later ovarian gene
of Y chromosome
action
th
Timeline 5 week begin as protuberances over the mesonephric ducts
4-6 weeks primordial germ cells move to these protuberances
6 weeks germ cells + mesenchymal cells (theca/leydig) +
epithelial cells (granulosa/sertoli)
Determin SRY
Lack of SRY + later ovarian gene
ant
action
Determin **Gonads** direct whether ductal system is male or
ant
female
Adult
Epididymis, vas deferens,
Fallopian tube, uterus, vagina
structur
seminal vesicle
es
Mullerian Sertoli cells -> Mullerian
No MIF (AMH) -> Mullerian system
system
inhibiting factor (AMH)
development
-> regression
Wolffian
Testosterone ->
Regression of Wolffian system
system
completion of Wolffian
system
Develop
Paramesonephric bulbs ->
ment
elongation, lateral fusion,
canalization, and septal
resorption
Hormone 5-alpha reductase: T ->
Lack of androgens -> feminization
s
DHT -> masculinization
of external genitalia
of external genitalia
Genital
-> Glans -> Penis
-> Glans -> Clitoris
Tubercl
e
Urogenit -> Urethral meatus
-> Vagina and urethra
al Slit
Labioscr -> Scrotum
-> Labia majora and minora
otal
folds
2. Given a defect in one of the basic steps for sexual differentiation, predict the end result for gonads,
the internal ductal system, and the external genitalia.
3. Describe one example of a disorder of sexual differentiation of each of the major categories of
abnormalities: genetic, gonadal, ductal, and external genitalia.
Step
Defect
Gonads
Genetic Sex
Turners (45X)
(lack of second X = cant
fully develop
ovary-> loss of oocytes)
Ovarian
streak
Formation of
Internal
Ductal
System
Uterus/vagina
External
Genitalia
Clitoris
Gonad
Formation of
Ductal
System
Differentiati
on of
External
Genitalia
Vaginal Agenesis
Ovary
(paramesonephric bulb
fusion defect)
CAH (21-OHase deficiency Ovary
in 46XX)
Absent
Clitoris
Uterus/vagina
Masculinized
DSD
CAH
5-alpha reductase deficiency
Androgen insensitivity
Inheritance
Autosomal recessive
Autosomal recessive
X-linked recessive
Delayed Puberty
1. Discuss common causes of delayed puberty in males and females.
Gender
Girls
Element
Breast Development
Menarche
Testicular enlargement
Boys
Delayed if after
13 years
15.5 years
13.5 years
Category
M F
Description
% %
Constitutio 60 30 Normal puberty 2.5 SD
nal Delay
% % delayed from mean
Hypogonad 30 40 Hypothalamus or pituitary
otropic
% % defects -> lack of normal
hypogonadi
GnRH and/or
sm
gonadotropin secretion
Etiology
None identifiable
Permanent: tumors/disease of
CNS, hypopituitarism,
chemo/radiation, idiopathic
Functional: systemic illness (IBD,
celiac), endocrine disorders
(hypothyroidism), stressors
(excessive exercise)
Defects causing failure of
ovarian/testicular function Turners syndrome, gonadal
dysgenesis, chemo/radiation,
synthetic defect, autoimmune
destruction, torsion
2. Discuss the significance of presence or absence of breast development and/or pubic hair in a female
patient presenting with a pubertal abnormality.
Breast Development
Pubic Hair
Developme
nt
Presen
t
Absent
Present
Normal
Absent
HPG axis aberrant
3. Compare and contrast the etiology of germ cell loss and associated findings of Turner syndrome in
females with Klinefelter syndrome in males.
Karyoty
pe
Epidem
iology
Stature
Second
ary
Sex
Charact
eristic
s
Klinefelter
Syndrome
Turner Syndrome
47, XXY
1/500 to
1/1,000
Tall,
eunuchoid
Gynecomast
ia
1/5,000
Short
Breast development with
normal pubic hair
46,XY
Gonadal
Dysgenesis
46,XY SRY
defect
Androgen
Insensitivi
ty
46,XY
mutant AR
Tall
Mullerian
internal
ducts, normal
female
external
Short
vagina,
ends in
blind pouch
Female
external
Gonads
Somati
c
Abnorm
alities
Gonadal
failure
(variable
severity)
Ovarian streak
NO puberty
Cardiovascular (aorta
problems)
Horseshoe kidney
Endocrine thyroiditis and
autoimmune diseases
Turner stigmata: webbed
neck, high palate, nail
hypoplasia, short 4th
metacarpal, multiple
pigmented nevi, other
Germ cell
tumors
Treat with
hormone
therapy
genitalia,
large
breasts
Testes
(internal)
Germ cell
tumors
4. Use the condition of idiopathic hypogonadotropic hypogonadism to discuss the signals for onset of
normal puberty.
Mutation/
Syndrome
GnRH
Receptor
FGFR1
Kallmans
Syndrome
Description
Phase
Day
Follicles
Follicular
1
Cohort of 2030 follicles
Hormone
s
Gonadot
ropins
Endomet
rium
Cycle
Length
Amount of
Flow
Withdrawal
of
E and P
Dominant
follicle
(arrested in
prophase)
Others die off
Estrogen
Shedding
14
Dominant
follicle ->
ovulation
VERY high
estrogen
LH Surge +
FSH
Proliferation, growth
Normal
22-45 days; median 27,
mean 29
20-45 mLs, 92% in first
2-3 days
Luteal
Corpus
luteum
(driver of
luteal
phase, VERY
high blood
flow)
Progestero
ne (from
CL)
Estrogen also
high
28
Corpus
luteum
withers with
no hCG
Secretion; compaction,
stabilization
Abnormal
Consistent loss of >80mLs, correlated with
passing large clots
Ovulat
ion
Endom
etrial
growt
h
Vascul
ar
chang
es
Endom
etrial
shedd
ing
Hormo
nes
Mense
s
Normal Cycle
Ovulatory
LIMITED growth, structurally
stabilized by hormones
PCOS Cycle
Adolescent Cycle
Anovulatory/Oligoovulator Anovulatory but
y
normal
Thickened, unstable,
Limited growth from
large quantity
unopposed
estrogen
Progressive vasoconstriction
and final hemostasis of
coiled arteries
Universal, limited
Erratic, non-universal
(potentially prolonged
and heavy), and
incomplete
Long term unopposed E
No feedback
Relatively limited
menses, universal
Intact negative
feedback between
FSH and estrogen
->
Regular (21-45
days), but variable
Irregular if regular
periods become
irregular or if
outside 21-45 days
4. Describe and explain the changes in gonadotropins that occur in the menopausal transition.
5. Contrast the differences in the differential diagnosis of abnormal uterine bleeding in teens compared
to older reproductive women.
6. Discuss the major categories of menstrual irregularity in reproductive aged women.
Anovulation/Oligo-ovulation (typically
YOUNGER)
Hypothal
amics
Psychogenic/stress/diet/exerci
se/body fat (MOST
COMMON), CNS tumors,
systemic disease
Endocrin
opathie
s
Other
7. Contrast the following terms and explain which ones would be expected to be associated with
anovulation or oligo-ovulation:
Dysfunctional
uterine
bleeding
Breakthrough
bleeding
Metrorrhagia
Menorrhagia
Menometrorrhag
ia
Primary
Dysmenorrhea
1.
2.
3.
4.
Physical
Features
Ovary
Chronic
anovulation
Androgen
excess
Obesity
Acanthosis
nigricans
Endocrine Normal GnRH
Changes
axis
FSH/E2
Negative
Feedback
System
PCOS
VICIOUS
CYCLE
Etiology
Insulin
resistance
Hypotheses
Risks of PCOS
Diagnosis
(Need
2/3,
hyperand
rogenis
m
most
importa
nt)
Hyperandrog
enism
Oligoamenorr
hea or
amenorrhea
Polycystic
ovaries by
US
EXCLUDE
Treatmen
t
Estrogen
Progesterone
Combined
hormonal
contraceptiv
es
Weight loss
Insulin
sensitizing
agent
Anti-androgens
Eflornithine
hydrochloride
Physical
removal of
hair
Ovulation
induction
treatments
(for
conception)
Defect of steroidogenesis?
Metabolic disorder?
Endometrial hyperplasia, T2DM, cardiovascular disease,
sleep apnea, dysphoria, depression, unwanted
pregnancy
Elevated blood androgen levels or physical signs
(hirsuitism, acne, etc)
Cycles less frequent than 35 days
12 or more follicles 2-9mm in size in one or both ovaries
CAH, Cushings syndrome, hyperprolactinemia, primary
hypothyroidism, acromegaly, premature ovarian failure,
simple obesity
Used high-dose short period of time in hospital, NOT by
itself long term
For abnormal uterine bleeding and amenorrhea
Suppress androgen production, SHBG, protects
endometrium
Good long-term conservative treatment
Treat glucose intolerance
Cyproterone acetate, spironolactone, flutamide (all are
teratogenic)
Topical inhibitor of hair growth
Treat hirsutism
Clomiphene citrate: acts as anti-estrogen
Letrozole: aromatase inhibitor
Gonadotropin therapy
Insulin sensitizing agents
Ovarian wedge biopsy/ovarian drilling damage theca
Female Infertility
1. Discuss normal fertility including the expected chance for pregnancy over 1 year and how that chance
for pregnancy changes as women age.
Probability of Conception
25%/cycle
10-15%/cycle
85%
% Infertile
11%
33%
87%
Percent Loss
12.2
14.3
13.7
15.5
18.7
33.8
53.2
Infert Definition
ility
Caus
es
Primary
infertility
Secondary
infertility
Male Factor
Disorders
Ovulatory
Disorders
Tubal,
pelvic,
endometri
osis
Testi
ng
Treat
men
Decreased
Ovarian
Reserve
Unexplaine
d
Overview
Overview
t
3. Describe factors that impact the chance to become pregnant.
a. Extremes of body weight
b. PCOS
4. Discuss the reproductive implications of increasing oocyte aneuploidy with age
a. Increasing rate of aneuploidy with aging due to impaired meiotic spindle formation -> rates of
chromosomally abnormal oocytes ovulated -> more spontaneous abortions
5. Discuss infertility care as an example of health care delivery issues
Emotional
Aspects
HCDS
Issues
Estrogen
follicular growth
Endometrial growth, maturation of vagina, cervical mucus
Androgens
Describe the synthesis and metabolism of androgens, the physiologic effects of androgens, age-associated
androgen deficiency, mechanisms of action of Androgens. Describe the clinical uses of androgens, including their
pharmacology, mechanism of action, clinical uses, adverse effects and contraindications.
2. Describe agents used for androgen suppression, including steroid synthesis inhibitors, 5-alpha reductase
inhibitors, anti-androgens, receptor inhibitors and selective modulators of androgen activity (SARMS).
3. Review the physiologic role of estrogen and progesterone in the female reproductive cycle. Describe the action of
synthetic hormones in oral contraceptives.
4. Describe the basics of the biosynthesis of estrogen and progesterone.
5. Recognize the pharmacologic uses of agents that affect the gonadal axis.
6. Discuss the effect of tamoxifen on estrogen receptors, the action of clomiphene on release of LH and FSH, the
action of mifepristone in blocking progesterone in pregnancy
Analog
Mechanism of Action
Use
ADRs/CIs
GnRH
Gonadorelin
Suppression of E/T production in
C/I in pregnancy
Disrupts GnRH pulsatility to
(Factrel,
hormone dependent
Males: diabetes, MI,
LH/FSH
Cystorelin)
breast/prostate cancer
IV
sudden cardiac death,
(respectively)
stroke
Goserelin
Highly bioavailable, more
Delay onset of precocious
(Zoladex)
stable than native peptide
Females: risk for bone
puberty
Naferelin
IN, SC, IM
mineral density, use nonDelay puberty in transgendered
(Synerel)
hormonal contraception,
youth
Leuprolide
not for nursing mothers
Hypergonadism
(Eligard)
LH
hCG
FSH
Pregnyl, follutein,
novarel
Menopur
Estrogen
Progester
one
Androgen
s
AntiEstroge
ns
T esters: Tproprionate,
-enanthanate,
cypionate
Alkylated T:
methyland
fluoxymesteron
e
Transdermal T:
Testoderm,
Androderm,
Androgel, Axiron
Tamoxifen
Orally active
Arimidex
AntiProgesti
ns
Mifeprostone
AntiAndroge
ns
Flutamide
Bicalutamide
Nilutamide
Stimulate ovulation
Contraception (mimics negative
feedback -> LH/FSH)
HRT
Male-to-female transgender
Support pregnancy with high risk
of miscarriage
thickening of uterine lining
caused by post-menopausal
estrogen
Androgen deficiency in aging
men, FTM transgender
Gynecologic disorders: postpartum breast engorgement,
endometriosis, chemo
Anabolic agent following trauma
or surgery
Osteoporosis
Growth stimulation (delayed
puberty in males)
Abuse in sports
Androgen receptor
modulators: block
activation of androgen
target genes
Orally active, rapidly
absorbed
Post-coital contraceptive
Abortifacient (1st trimester)
Finasteride
Dutasteride
Ketoconazole
Spironolactone
5- reductase inhibitors:
competitive inhibitor,
conversion of T to DHT
Steroid synthesis
inhibitors: non-specific,
will synthesis of other
steroid hormones
Endocrinology of Pregnancy
1.
2.
3.
4.
Describe the hormone interactions that maintain pregnancy in the early postimplantation stage.
Discuss fetal-placental-maternal interactions involved in steroidogenesis during pregnancy.
Describe placental protein hormones and PGs produced during pregnancy.
Recite examples of the clinical effects or uses of placental/pregnancy hormones.
Moth
er
Place
nta
Fetus
Pregn
ancy
Horm
ones
Maternal
endocrine
glands
Syncytiotroph
oblast
Cytotrophobla
st
Hypothalamic
pituitary axis
Measurement
Testing
hCG
Estrogen
Progesterone
Prostaglandins
Aneu
Overview
ploid
y
Scree
ning
AFP
hCG, Estriol
(E3), Inhibin
A
Partu
ritio
n
Steps
CRH
1.
progesterone, prostaglandins, distension,
estrogen, oxytocin
2.
Smooth muscle without gap junctions -> smooth
muscle with gap junctions
3.
Labor: coordinated contractions across uterus,
accompanied by cervical ripening and softening
Produced by placenta, can predict (in research studies) when
labor will begin
Leads to production of fetal cortisol, which placental CRH
production
Along with ACTH, -> fetal adrenal production of DHEA-S,
which is then converted to estrogen by placenta
estrogen levels mean ratio of E:P is shifted, also uterine
contractile response to oxytocin and fetal lung maturation,
cervical ripening
1.
2.
3.
4.
5.
Describe
Describe
Describe
Describe
Describe
adaptation
adaptation
adaptation
adaptation
adaptation
Plasma
Hematologic
RBCs
Dilutional
anemia
Total
blood
volume
Hypercoa
gulation
Immune
function
Overview
Cardiovascular
Heart
sounds
Cardiac
output
Vasculat
ure
Blood
pressur
e
Mucosa
Diaphrag
m
Ventilati
on
to
to
to
to
to
pregnancy:
pregnancy:
pregnancy:
pregnancy:
pregnancy:
GI
Renal
Respiratory
Arterial
blood
gas
Maternal
Hemorrha
ge
Antepartu
m
Maternal
Mortality Ratio
(MMR)
Main Causes
Overview
Placenta Previa
Placental
Abruption
Maternal
Hemorrha
ge
Postpartu
m
Overview
Main Causes
Risk Factors
Uterine Atony
Hypertensiv
e
Disorders
Preeclamp
sia
and
Eclampsia
Overview
Main Causes
Mild Preeclampsia
Severe
Preeclampsia
HELLP syndrome
Eclampsia
Pathophysiology
Systemic Effects
Of Preeclampsia
Infections
- Puerperal
Sepsis
Epidemiology
Definition
Cause
The number of maternal deaths within 42 days of a pregnancy per 100,000 live births
Hemorrhage, VTE, hypertensive disorders (CNS hemorrhage), indirect causes (CV disease,
non-obstetric injuries), infection
Antepartum hemorrhage: bleeding during an ongoing pregnancy that threatens the
wellbeing of the mother or the fetus
Definition: Placenta over cervix. Incidence 0.5%
Presentation: 70% present with painless vaginal bleeding, 20% with contractions +
bleeding
Risk factors: multiparity, AMA, prior placenta previa, multiple gestation, prior cesarean,
tobacco use
Diagnosis: ultrasound (transabdominal or transvaginal)
Definition: premature separation of normally implanted placenta, 0.5-1.5%
Presentation: complete abruption can result in fetal death; painful vaginal bleeding
in 80% (amount not correlated with amount of abruption), fetal HR usually non-reassuring
Concealed hemorrhage = blood dissects upward toward fundus without vaginal bleeding
External/revealed hemorrhage = blood dissects toward cervix
Diagnosis: ultrasound only 50% accurate, but used to exclude previa
Cause: hemorrhage into decidua basalis, which -> further separation, bleeding,
compression, and destruction; inciting cause unknown, but may be due to trauma
Risk factors: maternal hypertension, prior placental abruption, trauma, polyhydramnios,
premature rupture of membranes, tobacco use
Occurs in 4% of deliveries (immediately after), contributes to 20% of in-hospital maternal
deaths
Average blood loss <500cc vaginal, <1000cc with cesarean
Criteria: 10% drop in Hct, need for transfusion, or signs and symptoms
Uterine atony (80%), genital tract trauma, retained placental tissue, low placental
implantation, uterine inversion, coagulation disorders
Prolonged/augmented/rapid labor, h/o postpartum hemorrhage, overdistended uterus,
operative delivery, MgSO4, chorioamnionitis
Definition: failure of uterus to contract after placental separation and close blood vessels,
-> blood loss from myometrial spiral arterioles and decidual veins of intervillous spaces
Occur in 10-20% of pregnancies, with pre-eclampsia in 5-8%
Lead to 8% of maternal deaths in US, associated with CNS hemorrhage and stroke + fetal
and neonatal complications
Preeclampsia or eclampsia, chronic hypertension, gestational hypertension
New-onset hypertension (140/90) after 20 weeks in a woman with previously
normal BP, or new onset proteinuria 300mg/24 hrs after 20 weeks
BP 160/110 on 2 occasions at least 6 hours apart, or proteinuria 5g/24hr, or renal
insufficiency (Cr >1.1mg/dl), pulmonary edema, new onset cerebral disturbances,
epigastric/RUQ pain, liver function, thrombocytopenia
Hemolysis, Elevated Liver enzymes, Low Platelets a high morbidity variant of
preeclampsia
Tonic-clonic seizures in a woman with pre-eclampsia not attributable to other causes,
generally <24 hours post-delivery
Abnormal cytotrophoblast invasion + remodeling of uterine spiral arterioles at implanation
-> placental hypoxia/ischemia
--Current theory: imbalance in angiogenic and antiangiogenic proteins -> VEGF and PIGF +
sFlt1 -> endothelial cell dysfunction -> vasoconstriction + PGE2/NO,
PGF/TXA2/endothelin-1
CV: SVR, HTN
Renal: afferent arteriolar constriction, GFR, glomerular injury, proteinuria, ARF, oliguria
GI: hepatic necrosis/hemorrhage, liver enzymes, RUQ pain, hepatic hematoma
CNS: resistance of cerebral vascular blood flow, cerebral O2 consumption, h/a, vision
disturbances, seizures, encephalopathy, stroke
Hematologic: endothelial cell injury with capillary permeability, edema, IV volume
depletion, hemoconcentration, coagulation abnormalities
Respiratory: capillary permeability, pulmonary edema
Reproductive: uterine artery vascular resistance, pulmonary blood flow, nutrient/O2
delivery, abruption placentae
Occurs in 6-7% of vaginal deliveries, 10-15% of cesarians
A temperature of 100.4F or higher that occurs for more than 2 consecutive days during
first 10 postpartum days
Most common = endometritis (mixed anaerobe infection, caused by necrotic
endometrium/placental fragments -> favorable growth conditions), also from perineal and
cesarean wounds; 70% mixed anaerobic
Consequences
Risk Factors
Definition
Synonyms
Clinical
Diagnosis
Initiation
Power
Passage
Phas
es
Phase 0
Phase 1
Phase 2
The physiologic process by which the uterus expels, or attempts to expel, the fetus and placenta at 20
weeks or more of gestation
Parturition, childbirth, accouchement
Painful uterine contractions causing cervical effacement and dilatation
Unknown! Progesterone withdrawal, oxytocin, uterine stretch, prostaglandins
Fetal endocrine control (placental CRH and estrogen seem to be triggers, shift ratio of E to P)
Myometrium = interwoven bundles of smooth muscle cells in a spiral arrangement, matrix of collagen and
GAGs, gap junctions that allow rapid transmission of signals, marked in late pregnancy
Contractions pull up on muscles and out on cervix
Measured in intensity, frequency, and duration via palpation, IUPC, tocodynamometry
At height of contraction, uterus cannot be indented
External monitoring: tocodynamometer (measures contractions) + transducer (fetal heart rate)
Internal monitoring: use intrauterine pressure catheter + scalp electrode
GOOD CONTRACTION: covers entire uterus, gradient so all parts reach peak at same time, IUP 5060mmHg, frequency q2-4min, complete relaxation between contractions
Have different shapes and planes of pelvis as you move through. Ischial spines are typically rate limiting
factor
Fetal head: bones arent fused together so baby can fit through; flexion of head produces lowest
diameter
Lie: long axis of fetus to long axis of mom (longitudinal, oblique, transverse); typically settle by 36 weeks
Presenting part/presentation: what can be felt on vaginal exam, a point of reference (cephalic, breech,
shoulder)
Position: relationship of baby part to four quadrants of maternal pelvis (OA, ROT, OP, LOT [O=occiput])
Attitude: relationship of fetal parts to itself (flexed, military, extended)
Station: how far babys head is engaged in pelvis
Leopold maneuvers: can tell multiple aspects of babies lie, presentation, position, attitude
Cardinal movements: engagement, flexion, descent, internal rotation, extension, external
rotation, expulsion
Pregnancy: Functional quiescence; inhibitors include progesterone, prostacyclin, relaxin, NO
Uterine priming: Release of inhibition as well as estrogen (a uterotropin) -> ion channels, gap junctions
Stimulation: uterine irritability PGE2, PGF2, oxytocin
3. Describe the pattern of normal labor, including its stages, mechanism, duration, and management.
Stag
e
Prod
rom
e
Stag
e1
Stag
e2
Stag
e3
Tim
e
Day
s
Prelabor changes
Cervical ripening: collagen chains fracture, more hydrophilic GAGs,
H2O -> softer, thinned out
Lightening: dropping, babys head engages with pelvis, -> room
to eat/breathe, urination
Passing the mucus plug (may be bloody)
Braxton-Hicks contractions: from 10 weeks on, non-propagated,
may not be felt
10
From beginning of labor until full cervical dilation (10cm)
hrs Initial phase: when cervix isnt doing much; Active phase: effaced
cervix
Cervical effacement: obliteration of canal/thinning of cervix
Cervical dilatation: enlargement of cervical opening
Fetal descent: to lower station (i.e. through pelvis)
Pain: contractions -> cervical dilatation (hypoxia, nerve compression,
peritoneal stretch) -> visceral afferents (sympathetic) to T10, 11, 12
30
From full dilation to delivery of fetus; the pushing stage
mi Pain: distention of pelvic, floor, vagina, perineum -> sensory branches
n
of pudendal nerve (S2, 3, 4); treat with pudendal block or local
anesthetic
5
From delivery of fetus to delivery of placenta and membranes
mi
n
4. Recognize the existence of abnormal labor patterns and abnormal fetal presentations, possible
causes of these abnormalities, and possible management options.
Contractions
Interval
Walking
Pain
Sedation
True Labor
Regular
Decreases
Makes worse
Abdomen AND back
Has no effect
Power
Causes
Uterine dysfunction
Passeng
er
Passage
False Labor
Irregular
May stay the same
Make make better
Abdominal
Subsides
Solutions
Augmentation, pain relief,
amniotomy
Change maternal or fetal position
Change maternal position to open
pelvis
Normally performed by
Lung
RES
Bone marrow
Liver
Endocrine
Temperature homeostasis
GI tract
Kidney
Ectopic pregnancy
Spontaneous abortion
Definitio
n
Prevalen
ce
Types
Fetal
Cause
s
Matern
al
Cause
s
Definitio
n
Incidenc
e
Sites
Causes
Histolog
y
Pre-Eclampsia
Complete
hydatidifor
m mole
Preval
ence
Pathol
ogy
Partial
hydatidifor
Preval
ence
m mole
Choriocarcin
oma
Managemen
t
Pathol
ogy
Preval
ence
Outco
mes
Other
Overv
iew
Clinical Contraception
1. Describe the component/s of a combination birth control pill, contraceptive patch, contraceptive ring,
birth control shot (medroxyprogesterone acetate contraception), IUDs, implants, and emergency
contraception.
2. Identify the mechanism of action of combination birth control pills, rings and patches, IUDs, and
emergency contraception in preventing a pregnancy.
3. Recognize the absolute contraindications to estrogen containing hormonal contraceptives in
clinical patient cases.
4. Discuss the difference in clotting risk between progestin only contraception and estrogen containing
contraception.
5. Apply knowledge regarding side effects, pathophysiology, and efficacy (e.g. menstrual pattern
changes), duration of action (e.g. Depo-Provera), special considerations( e.g. BMI in patients using
patch, active cervicitis in IUDs) in counseling patients regarding their potential appropriate and
optimal contraceptive choices.
Hormones
Combin
ation
OCP
Ethinyl
estradiol +
MANY different
progesterins
Low dose if
<35g EE (ALL
should be low
dose unless
specialized)
Continuous: ->
inhibited Gn
secretion
Contra
150 mcg
Mechanism of
Action
Progestin = main
component, LH
surge ->
ovulation; also
mucus; ->
endometrial and
ovarian cancer
Estrogen =
potentiates
progestin action ->
dose, better cycle
control by friability
of vessels, inhibits
follicular
maturation by
FSH
28 pills > 21 pills
forgotten doses
Less effective
Adverse Effects
P = androgenic (modern
generations = less androgenic)
Absolute contraindications:
1. Thromboembolic
disorders
2. liver function
3. Abnormal vaginal
bleeding
4. Pregnancy
5. Smokers >35
6. Known/suspected
breast cancer
Thrombosis = estrogen
dependent (NO risk with
progesterone), MUST ask
about clotting history!
Relative contraindications:
often not as relevant; surgery,
DM, Gb disease, migraines (if
ceptiv
e
Patch
Contra
ceptiv
e
Ring
Birth
Contr
ol
Shot
IUD
Norelgestromin
20mcg EE
>90kg women
Ethinyl Estradiol
Etonogestrel
Risk of pregnancy if
out >3hrs
Medroxyprogester
one acetate
Injections q3months
Copper (non
hormone)
Inflammatory reaction
prevents
fertilization
Makes cervix
inhospitable to
sperm
Lasts 3 years
Levonorgestrel
Implan Etonogestrel
ts
Emerge Levonorgestrel
ncy
(~4x higher
Contra
dose than OCP)
ceptio
n
Delay/stop follicular
maturation
Does NOT block
fertilization or
interrupt after
implantation
85% effective if taken
within 72hrs
6. Formulate a counseling conversation to accomplish the following: You are a clinician and advising a
21 year old regarding contraception. She is set on using an oral contraceptive pill. She has no
contraindications. How will you conduct an interactive counseling session rather than a lecture on
oral contraceptives? What anticipatory guidance will you give her? How will you attempt to decrease
the chance she will discontinue the oral contraceptive? How would you maximize the chance she will
remember to take her pills daily?
Method
Tubal sterilization
Male condom
Vasectomy
Three-month injectable
Pill (combined)
IUD Copper
IUD Mirena
Periodic abstinence
One-month injectable
Implant
Patch
Emergency
Contraception
Diaphragm
Withdrawal
No method
Perfect
Use
(%/yr)
0.5
2
0.1
0.3
0.3
0.6
0.1
1-9
0.05
0.05
0.3
Typical
Use
(%/yr)
0.5
15
0.15
3
8
0.8
0.1
25
3
0.05
8
15
6
4
85
16
27
85
Continuation
Rates
(age 15-24)
% Use
17%
11%
16%
30%
19%
85%
11%
3. Cite an example of a health care disparity related to unintended pregnancy rates or contraception in
the US.
a. Highest in women age 18-24, unmarried women, low income women, women who had not completed high
school, and minorities
4. Recognize/apply strategies that would increase utilization of contraception to meet the goal of
decreasing the unintended pregnancy rate.
a. Education about contraception
b. Sexual education in schools
i. Abstinence only education in use does not work no delay in activity + no increased contraceptive
use
ii. Educating skills (ways to say no to sex) works
iii. Making contraception a societal normative responsibility for both teen male and female
c. Providing free condoms @
d. Increase IUD or other LARCs @
e. Parents who talk about sex are more likely to have abstinent kids discuss values, latchkey coitus,
spend time, understand normal adolescence
f. Improve utilization of OCPs memory cue to take OCP
i. Also discuss what problems they had remembering, concerns, finances, BTB/amenorrhea; call if
decide to quit
5. Discuss the issue and give an example that may be interpreted as gender bias as it applies to
contraception.
a. Legislation allows employers to opt out of coverage if they are opposed to contraception
b. Gender bias more marked in low SES women in poverty 6x rate of failure of contraceptives than women
at 200% of poverty level
c. Viagra vs. contraception coverage inconsistencies both are lifestyle drugs
Anatom
y
Embryol
ogy
Location
Arterial
supply
Venous
drainage
Lymphatic
drainage
Overview
Mammo Childhood
genesis
Puberty
Menstrual
cycle
Adult
Pregnancy
Menopause
Lactoge
nesis
Prerequisites
Hormones
Milk factory
Stage 1
Stage 2
Stage 3
Advanta
ges
Of
Breastf
eeding
Immune
function
Customizatio
n
Improved
health
outcomes
Mother
Issues
with
Breastfe
eding
Contraindic
ations
Rates
Obstacles
Nursing
difficulties
Cyclic
Breast
Pain
NonCyclic
Breas
t Pain
ExtraMam
mary
Breas
t Pain
Epidemiology
11% of
premenopausal
women
Age 30-40s
Requires no
additional w/u
Age 40-50s
Focal pain or PE
finding ->
diagnostic
evaluation,
mammogram, US
Diagnostic
Technique
Physical
Exam
Mammogra
phy
Ultrasound
MRI
Biopsy
40%
Etiology
Unclear
Presentation
Most have spontaneous
resolution
Starts in luteal phase,
dissipates with menses
Diffuse, bilateral pain, can
radiate to axilla
Unilateral, localized to one
quadrant
Trauma, thrombophlebitis,
mastitis, medications,
benign tumors, cancer,
often idiopathic
Musculoskeletal: costochondritis, chest wall pain,
fibromyalgia, cervical radiculopathy, shoulder pain, VZV,
pulmonary embolism, pleurisy
Details
Ask about pain, character, periodicity, relation to menses
Palpate breasts for dominant mass, include neck, chest, regional lymph
nodes
Pay attention to growth asymmetry. Look for dominant masses!
hardness, definition, mobility, size
Also look for nipple discharge, skin changes
DO NOT IGNORE CLINICAL FINDINGS EVEN IF EXAM IS
NEGATIVE!!! MUST GET BIOPSY
NOT perfect; 20% FNR (40% in young women with dense breasts)
neg. mammogram + palpable mass = uninformative
Look for microcalcifications, new densities, asymmetry
Differentiate solid vs. cystic; adjunct to mammogram
For women at highest levels of risk. Also before surgery
Indicated in patients with suspicious physical exam and normal
imaging
Recommend core biopsy rather than FNA for all breast pathology
Guidance: US, stereotactic (mammography), or MRI; surgical (if
imaging normal); blind (if huge tumor)
Path report: correlates with imaging findings, includes risk of
developing cancer, additional imaging, surgical needs
25%
25%
9%
1%
Malignant Neoplasms
Carcinoma
Ductal Carcinoma (non-special)
Ductal Carcinoma (special)
Tubular
Medullary
Papillary
Mucinous
Lobular Carcinoma
Pagets disease
Inflammatory Carcinoma
Sarcoma
Benign neoplasms
Fibroadenoma
Intraductal papilloma
Lipoma, granular cell tumor
Inflammatory Disorders
Acute mastitis
Periductal mastitis
Duct ectasia
Fat necrosis
Lymphocytic mastopathy
Granulomatous mastitis
Mondors Disease
Developmental, Hypertrophy Disorders
Benign
Lesions
Fibrocysti
c Disease
99%
75%
11%
6%
2%
1%
2%
10%
2%
2%
1%
62%
25%
13%
Risk
Presentation
Management
Histology/Imaging
Understanding
and support
Non-narcotic
analgesics,
diuretics,
hormones
Subcutaneous
mastectomy
Proliferati
ve with
atypia
RR of
BC
4-5x
Proliferati
ve
without
atypia
No
risk
of BC
RR of
BC
1.52x
Acute
Mastitis
Periductal
Mastitis
Surgery to
exclude
malignancy,
then watch
Inflammatory Disorders
Lactational staph/strep
Abx, continued
milk
expression
Rarely surgical
drainage
Recurrent subareolar abscess
Drainage +
Abx, smoking
cessation
Epithelial hyperplasia
Sclerosing adenosis
Complex sclerosing
lesion (radial scar)
Papilloma (80% w/
nipple discharge)
Atypical ductal or
lobular hyperplasia
Flat epithelial atypia
Keratinizing
squamous
metaplasia
Duct
Ectasia
Mimics cancer on
mammography
calcifications, architectural
distortion, nipple retraction
Fat
Necrosis
Lymphocy
tic
Mastopat
hy
Granulom
atous
mastitis
Mondors
Disease
Total duct
excision if
recurrent
None
Duct dilation,
inspissated
secretions,
periductal
inflammation
Self-limiting
Only
symptomatic
tx prn
Lymphocytic infiltrate
surrounding ducts
and blood vessels
Non surgical
Steroids if
refractory
Warm packs
Ibuprofen
Superficial
thrombophlebitis of
the veins of the
anterior chest wall
1.
2.
3.
4.
Breast Malignancy
1. Identify the most important epidemiology / risk factors for breast cancer.
Age
Estrogen
exposure
Family history
Prior cancer
Prior radiation
Biopsy
Obesity
Alcohol
2. Apply the different breast imaging techniques depending on the clinical circumstances. (see previous
lecture)
3. Differentiate the varying types of breast carcinoma and their prognostic implications based on the
different pathology sub-classifications.
Lobular
Ductal
Ductal
Carcinoma
in Situ
(74%)
Ductal
Carcinoma
(74%)
Lobular
Carcinoma
in Situ
Prognosis
50% chance of invasion with
recurrence
Treat as cancer
Findings/Histology
Most common finding on
screening mammogram
(non-palpable)
Non-invasive
Linear, pleomorphic
calcifications in one
breast on mammography
Diffuse malignant
calcifications
Nipple inversion
Blockage of lymphatics ->
peau dorange
Treatment
Excision! local radiation
Local control: eradication of all known
tumors within breast and regional nodes
(surgery, radiation therapy, neoadjuvant
chemo)
Systemic control: aka systemic adjuvant
therapy; tamoxifen
Targeted therapy: use of anti-tumor
treatments that interfere with specific
targeted molecules/pathways needed for
tumor growth
Also use radiation + chemo + systemic
adjuvant therapy + excision
Surgery to exclude malignancy, then close
surveillance
L. Carcinoma
Prognostic factor: factor which imparts an equivalent relative benefit (or risk) regardless of whether the patient
receives treatment or not
Predictive factor: factor which imparts a relative benefit in terms of improved response to a specific treatment
(Her2+ = Herceptin susceptible)
Type
Luminal A
Luminal B
Basal-Like
Her2/Neu
Positive
% of
DCs
40-55%
15-20%
13-25%
E
R
+
+
-
P
R
+
+
-
Her2/Ne
u+
-
7-12%
Details
Responds to hormonal treatments
Higher grade and proliferative activity
Expresses myoepithelial markers; a/w
BRCA1
Higher grade and proliferative activity
4. Identify the treatment choices for non-invasive breast cancer, localized (non-metastatic) invasive
breast cancer, and metastatic breast cancer.
Non-
Local Therapy
Invas
ive
Systemic
Adjuvant
Therapy
Follow Up
Localized (NonMetastatic) Invasive
Metas
tatic
Overview Definition
Epidemio
logy
Overview
VictimPerpetrator
Relationship
s
Co-morbid
Findings
Determinant
of health
Professio Reporting
nal
Obligations
Respon Clinician
se
Resources
Principles for
Safety and
Discharge
Clinical
Skills
Normal
Prepubertal
Female
Genitalia
Exam
Findings
Symptoms
(red flags)
Disclosure
2. Identify acute injuries associated with IPV and SA and discuss the required documentation, testing
and treatment (prophylaxis) associated with the acute evaluation.
3. List long-term consequences (physical, emotional, and overall health status) of IPV and SA.
4. Discuss the prevalence and social context of IPV and SA.
5. Describe the overlap of IPV and SA with other major problems, including child abuse and substance
abuse.
Definitions
Demograph
y&
Prevalenc
e
Crimes
Health
Conseque
nces
Evaluation
&
Document
ation
Treatment
Response
Perpetrator
s
Signs/Symp
toms
Victim
Blaming
Responding
with
Empathy
Sexual Violence
Non-consensual sexual contact by coercion, physical force, threat of
bodily harm, or when consent is not possible
A range of cultural messages and personal behaviors, which includes
coercion, manipulation, pressure, and violence that violates personal
boundaries and/or persons right to choose, with the intent of gaining
power and control over another person
Majority associated with use of EtOH/drugs. <50% reported. 6%
offenders ever spend time in jail.
Focus = power and violence. Progression of offenses (voyeurs ->
rapists). Incestuous families
Acute distress -> depression, exhaustion, restlessness -> PTSD.
Disruption of relationships -> sexual dysfunction. Chronic pain,
hypersexuality, revictimization. use of medical services. health
status.
Need careful, accurate history. Privacy + Consent + Chain of evidence
+ Encourage reporting.
Complete physical exam as per rape exam kit
Treat acute injuries. Test for STDs, pregnancy. Involve support agencies
(WISE), police. Follow up.
Interpersonal Violence
Controlling, possessive, entitled, manipulative. Disrespect partner.
Confuse abuse and low. Strive to have good public image.
Deny/minimize abuse
Bruising/burns, malnutrition, frequent illness, isolation, extreme anxiety,
depression, neglect, STDs
Victims face barriers to reporting must support them! Why does he
do this? vs. Why doesnt she leave? (<- victim blaming)
Victim is the best expert on her safety. Do believe, listen, respect,
and refer.
Adolescent Sexuality
1.
2.
3.
4.
5.
Develop Overview
mental Preadolesc
Change
ent
s
Early
Adolescen
t (10-13)
Epidemi
ology
Middle
Adolescen
t (14-16)
Late
Adolescen
t (17+)
Added
Risks
LGBTQ
Key Points
Issues
Confide Laws
ntiality Age of
Majority
Emancipate
d minor
Mature
minor
doctrine
Age of
Consent
Exceptions
STIs
Risk factors
Screening
Strengt
hening
Overview
Sexual
Health
Choices
Prevention
Techniques
Abortion
1. Describe the different types of abortions.
Abortion
Viability
Induced
abortion
Safety
Benefits
of Legal
Abortion
Rights of
a Patient
Rh
Prophyla
xis
Aftercare
2. Compare the different methods for performing first and second trimester elective pregnancy
termination.
Type
Description
Requirements
First Trimester Abortion
Manual Uses modified syringe
Early recognition of
Vacuu
that creates a vacuum,
pregnancy 5-10
m
hooked up to a cannula,
weeks from LMP
Aspirat
suction -> termination of Cervical dilation if
ion
pregnancy
>6mm cannula used
Simplest, safest, least
Rh prophylaxis!!!
expensive
Examination of aspirated
tissue is essential
Complications
0.7% pelvic infections
0.5% retained
products of
conception
Need for repeat
aspiration
V. rare uterine
perforation
Dilatio
n and
Curett
age
Removal of pregnancy
contents by mechanical
means (vacuum most
common)
Usually performed in
freestanding clinics
Medica
l
Aborti
on
<12-13 weeks
gestational age
Dilation of the cervix
Premedication with
NSAID
Local, spinal, or
conscious sedation
<9 weeks gestational
age
Mifepristone
progesterone antagonist,
600mg single oral dose
Misoprostol on day 3,
400mcg PO/intravaginal
Patient then remains in
clinic for 4 hours
expulsion of pregnancy
Second Trimester Termination
Dilatati Mechanical and suction
Laminaria: take up
on
removal of formed
water from cervix +
and
pregnancy after cervical
exert gentle pressure
Evacua
dilation
-> dilation
tion
Can pre-inject IU
abortifacients to
terminate fetus
Prosta Typically misoprostol
glandi
n
Suppos
itorie
s
IV
Also effective
HighDose
Oxytoc
in
Hyster Surgical method remove (Not done)
otomy
pregnancy abdominally
Higher complication
rates
Risk of water
intoxication
3. Discuss the common complications that can arise as a result of having an abortion.
Complication
Cervical Shock
Cervical
Lacerations
Uterine
perforation
Hemorrhage
Post-Abortal
Syndrome
Description
Vagal response to dilation of cervix patient passes out
Occur when dilating cervix too quickly
Blind procedure, so can puncture uterus
From uterine perforation or uterine atony
Uterus doesnt sufficiently contract, fills up with clots -> swollen
abdomen
Urinary Incontinence
1.
2.
3.
4.
5.
6.
7.
8.
9.
Identify and name the major anatomic and histologic features of the bladder and urethra in the male and female.
Define incontinence.
Describe the epidemiological features of incontinence.
Describe the natural history and progression of incontinence.
List the risk factors for incontinence.
Recite the important components of the history when interviewing a patient with incontinence and the physical exam of a patient
with incontinence.
Discuss the laboratory, radiologic, or urodynamic tests, if any, that should be ordered in a patient with incontinence.
Identify the indications for treatment of incontinence.
Discuss the nonsurgical treatment options for stress and urge incontinence, describe their side effects, and outline the
mechanisms by which they work.
Incontin
ence
Innervati
on
Symptom
Sign
Parasympathe
tic
Sympathetic
Somatic
Overview
Risk
Factors
Reversib
DIAPPERS
le
causes
Constant Incontinence
Mixed incontinence
Evaluati
History
on
Physical
Urinalysis
Treatme
nt
Voiding
Diaries
Pad test
Post-void
Residual
Urodynamics
Presumptive
First Line
Behavioral
Devices
Drugs
FollowUp
Overview
Stress
Overflow
Urge
incontinenc
incontinenc
Incontinenc
10. List the symptoms and signs of the various types of incontinence: stress, urge, overflow, and mixed.
Cause
Bladder dysfunction
detrusor
overactivity of
neurogenic or nonneurogenic origin;
poor compliance of
bladder
Bladder
hasnt
emptied, is always
somewhat full
Anatomic (mobility of
bladder neck) or
intrinsic sphincter
deficiency (bladder
neck dysfunction)
Particularly with
hormonal changes,
Occurs when
Urgency! Without
warning, on the
way to to the
toilet, around
water, when full,
bedwetting
Extremes of
bladder fullness
dribbling,
frequency,
nocturia,
urgency; stress
maneuvers
Coughing,
laughing,
sneezing,
walking, bending
over, getting out
of a chair
Pathophysiology
Detrusor overactivity: bladder
pressure > sphincter ability;
idiopathic (elderly/obstructed)
or neurogenic (suprasacral
lesions)
Poor compliance: incremental
Obstruction:
women
rise in pressure
with (RARE
volume,
prolapse, post-suspension);
men (prostate disease, urethral
structure)
Poor contractility: DM,
longstanding obstruction, spinal
injuries, radical
pelvic
surgery,
Anatomic:
Descent
of bladder
from weak pelvic floor ->
increase in pressure from
intra-abdominal pressure + NO
increase in pressure on urethra
-> leakage
Conservative Tx
Complete bladder
emptying (clean
intermittent
catheterization
Anticholinergics
Alpha-antagonists
Complete bladder
emptying (clean
intermittent
catheterization)
Timed voiding
Indwelling
catheter
Pelvic
floor
exercises
Weight loss
Pessary
Alpha-agonists,
estrogen,
antidepressants
Surgical Tx
Tx obstruction
Botox
Nerve stimulation
turn it up turns
it off
Augmentation
cystoplasty
Relieve
obstruction
Mesh or fascial
slings not a
problem if done
and followed
correctly
Submucosal
injection to
Epidem
iology
Conseq
uence
s
Baby Blues
Prevale
85%
nce
Risk
Childbirth
Factor
s
Sympto Mild postms
partum mood
disturbance,
lasting <2
weeks
Conseq
uence
s
Treatm
ent
Postpartum Depression/Anxiety
10-20%
Postpartum
Psychosis
1-2/1000
Weight risks
vs. benefits
a.
b.
c.
Pregnancy
Untreated illness vs.
Treatment
Untreated illness =
adverse exposure
Breastfeeding
Treatment vs. Not breastfeeding
No clozapine (-> agranulocytosis), lithium
needs extra monitoring
No RCTs most data retrospective and observational, with lots of confounders (but more data on SSRIs
than many other commonly used meds in pregnancy); few studies control for degree of psych symptoms
No decision is risk free going without meds carries its own risk, but absolute quantification of risk is
impossible
Safest medication often the one that results in full remission of symptoms if you take a med, might
as well have it work!
d.
e.
f.
g.
h.
i.
j.
Use older medications with more data (fluoxetine, sertraline, citalopram), but base choice on past
response
Use lowest effective dose of single medication if possible
Do not taper prior to delivery
Consider non-medication somatic treatments
Therapy almost always first line, but hard to come by
High relapse rates for MDD, BPD if meds discontinued during pregnancy
Must consider individual illness history (how bad is illness?), response to meds (little benefit probably
not worthwhile), beliefs and preferences about meds during pregnancy, and obstetric risk factors
Punctatio
n
Acetowhi
te
Treatm
ent
3.
CIN I
CIN II/III
Learn the common presentation of a bartholins gland cyst/abscess, and provide proper management. (no questions
on this)
Bartholins Gland Problems
Norm
Function
Secrete mucus, moisture to vulva; located at 4 and 8 oclock positions of vaginal orifice; 0.5 cm in size
al
Absce
ss
Pathophysiolo
gy
Treatment
Long-Term
Cyst
Pathophysiolo
gy
Findings
Treatment
Epidemi
ology
Sympto
ms
Physical
exam
Radiogr
aphic
Treatme
nt
Leiomyoma
Caucasian women; black women, highest in 5th decade of life
Abnormal uterine bleeding (size + position in wall), pain, pelvic pressure,
lower urinary complaints ( frequency)
Reproductive complications: implantation, pregnancy; miscarriage
Enlarged, firm, non-tender uterus, irregular contour; if >12 weeks gestation
size, can palpate in abdomen
US: most common, least expensive
MRI: more expensive, excellent accuracy; useful in some circumstances
Expectant management
Medical management: hormonal (OCPs, Mirena - bleeding), NSAIDs (
pain with menses)
GnRH analogues: fibroid size by chemically inducing menopause;
very expensive, only approved for 6mo
--Used to reduce fibroid volume preoperatively, or as a bridge to
menopause in perimenopausal patient
Surgery: myomectomy or hysterectomy
--Can also do uterine artery embolization selectively occlude the arterial
blood supply to the fibroid
Endometrial Hyperplasia
Simple
Hyperpla
sia
Aden
oCa
?
1%
4. Understand the etiology of salpingitis and the significance of hydrosalpinx, an important clinical
sequela.
Salpingitis
Definit Inflammation of the fallopian tube; most commonly from ascending infection
ion
(PID)
Diagno Abdominal tenderness rebound, adnexal or cervical motion tenderness, +
sis
>1 of:
--T > 38, WBC > 100,000, pelvic abscess on imaging, pus on culdocentesis or
laparoscopy
Histol
Acute salpingitis: edema with mixed inflammatory infiltrate
ogy
Organi C. trachomatis and N. gonorrhea most common; less common =
sms
Mycoplasma, Streptococcus, Staphylococcus, Haemophilus, Bacteroides, E.
coli, Peptostreptococcus, Clostridium, Actinomyces
Hydro
Fluid in fallopian tube -> Very dilated lumen, fewer folds, compression of
salpi
muscular layer
nx
Benign
1.
2.
3.
4.
Functional Structures
Germ Cell
Stromal
Epithelial
Pre-Pubertal
-Mature teratoma (most
likely)
---
Reproductive Age
Follicle cyst
Corpus luteum
(combined = most common)
Mature teratoma
Post-Menopausal
--
-Serous cystadenoma
Mucinous cystadenoma
Fibroma
Serous cystadenoma
Mucinous cystadenoma
Mature teratoma
Malignant
Secondary
Involvement
Germ Cell
Stromal
Epithelial
Metastatic
--
Endometrioma
--
Dysgerminoma
(most common malignant)
(looks solid on US)
Dysgerminoma
Immature teratoma
Endodermal sinus tumor
Embryonal tumor
Choriocarcinoma
-Serous, mucinous
(low malignant potential)
Endometrioid, clear cell
carcinoma
Serous adenocarcinoma
Non-ovarian malignant tumors
2
3
4
Infec Bacte
tion
rial
CIN
III
Ca IS
Inva
siv
e
SCC
Cytol
ogy
Definiti
ons
Menopause
Postmenop
ausal
Perimenopa
use
Epidemi
ology
Premature
menopaus
e
Early
menopaus
e
Overview
Earlier with
Menstr
ual
Chang
es
Short
cycles
Interspers
ed
normal
cycles
Luteal
insufficie
ncy
After age 40, ovarian follicles become less response to FSH ->
fewer oocytes available in early follicular phase -> inhibin
and estradiol -> FSH levels -> dysfunction of corpus
luteum -> progesterone secretion -> heavier menses
Anovulatio Accelerated decline in follicles -> anovulation -> cycle
n
length and variability
--Bleeding from fluctuations in E level. Episodes spread out
and then stop.
Sympto
ms
PostMenopau
sal
Hormone
s
Vasomotor
symptom
s
Skin
Changes
Genital
Tract
Psychologic
al
Somatic sxs
Weight gain
Osteoporo
sis
Coronary
heart
disease
Treatme Reassuranc
nt
e
Menorrhagi
a
Comfort
measures
Nonhormone
Vaginal
Estrogen
Hormone
Replacem
ent
Therapy
Linear
Model
(Masters
and
Johnson)
Circular
Model
Biopsych
osocial
Model
Excite
ment
Platea
u
Orgas
m
Resolu
tion
Biology
Psychol
ogy
Sociocu
ltural
Interpe
rsonal
Overvie
w
Clitoris
Increases in
length
Retracts under
clitoral hood,
very
sensitive
Labia
Increase in
size, separate
outward
Vagina
Begins to
lubricate,
lengthen, and
distend
Minor lips turn
Entrance
bright red and
contracts,
increase in
barrel
size
expands
Strong
contractions
Other
Uterus and
cervix pull
up and
away
Uterus also
contracts
Overview
Distres
s
Prevale
nce
Risk
Factor
s
Female
Sexual
Interest/Aro
usal
Disorder
Descrip
tion
Etiolog
y
Desire
vs.
Arous
al
Female
Orgasmic
Disorder
Genitopelvic
Pain/Penetr
ation
Disorder
Sexu
al
Histo
ry
Treat
men
t
Appro
ach
Difficu
lties
Langu
age
NonPhar
m
Medic
ation
s
Conge
nital
Anato
mic/
Struct
ural
Infecti
ous
Inflam
mator
y
Tramat
ic
Vascul
ar
Benign
Neopla
stic
Malign
ant
Neopla
stic
Hypospad
ias
Epispadia
s
Phimosis
Paraphim
osis
Penile Disorders
Proximal urethral meatus + hooded foreskin + chordee
(curvature). DO NOT CIRCUMCISE!
Urethra on dorsal surface of penis. Very rare! Bladder can form
on outside of body.
Narrow contraction of tip of foreskin. 90% can fully retract by
age 3
Entrapment of the uncircumcised prepuce behind glans penis.
Prevent by ALWAYS returning uncircumcised foreskin to
normal position!
STD
Balinitis
2. Recognize that a solid testicular mass is a tumor until proven otherwise. A scrotal ultrasound is a
simple and reliable test to identify masses that are likely to be tumors.
3. Discuss the significance and pathology of cryptorchidism and hydrocele.
Caus
es
Skin
Tunica
Vas
Deferens
/ Cord
Scrotal Mass
Sebaceous cyst, Infections
Hernias. Hydrocoele: tunica vaginalis on surface of testicle swells
up, fluid-filled. Unknown cause
Varicocele. Post-vasectomy granuloma
Evalu
atio
n
Epididymi
s
Testis
History
Exam
**Scrotal
Ultrasou
nd**
Conge
nital
Infectio
us
Inflam
mator
y
Neopla
stic
Traum
atic
Vascula
r
(Torsion
)
Anato
mic/
Struct
ural
Not many
Epididymitis: kids = congenital, E. coli; young men = STI (chlamydia, GC);
older men: associated UTI, E. coli, Pseudomonas
--Pathogenesis: infection ascends -> vas deferens/lymphatics ->
epididymis/testis
--Pathology: acute = suppurative abscess, chronic = fibrosis/scarring
Orchitis mumps (viral), TB (caseating granulomas), tertiary syphilis
(gummas, diffuse inflammation)
Fouriers gangrene: need significant debridement! Cellulitis, fasciitis,
crepitus -> Rapidly extends
Henoch-Schonlein Purpura: vasculitis in kids, preceded by viral infection,
caused by IgA deposition in vessels; -> associated swelling of testicle
Tumor rupture VERY rare. Cancer typically does NOT present as acute
scrotum
Testicular contusion, rupture, or hematocele
Testicular torsion: surgical emergency! If you dont de-torse, can lose
testicle. Sudden severe pain! Diagnose with ultrasound look for blood
flow (will be absent).
--Occurrence: highest in neonates (in utero, shortly after birth) and
adolescence (commonly a/w bell clapper anomaly, may occur in sleep)
--Pathogenesis: twisting of spermatic cord cuts off venous drainage to
testis -> hemorrhagic infarction
--Pathology:
Other: Torsion of appendices of testis/epididymis. Testicular infarction:
Incarcerated hernia: bowel stuck
Strangulated hernia: bowel twisted and losing blood supply
4. Recognize that cryptorchidism (an undescended testis) is a risk factor for testis cancer
5. List the 2 primary pathological sub-classifications of germ cell tumors: Seminomas and Non
seminomatous germ cell tumors
6. Name the 2 primary tumor markers that germ cell tumors produce and that can be measured in the
serum: Alpha feto protein and Beta human chorionic gonadotropin.
7. Recognize that pure seminomas never produce alpha feto protein.
8. Outline the WHO classification of testicular germ cell cancers. (tumors of one type versus multiple types)
9. Describe the importance of serologic markers for testicular cancer.
Stagi
ng
Treat
men
t
Spermatoc
ytic
Seminom
a
TNMS
Stage I
Disease
Stage II
Disease
Stage III
Disease
Overview
Seminom
a
NSGCT
adulthood (usually
nodular, solid,
elements from all
mixed, has
and cystic
embryonal layers, can
malignant
be functional or ->
potential)
secondary malignancies
Benign, in older
Looks different from usual
men, NO
seminoma!
malignant
transformation
Tumor, nodes, metastases, serum markers
Limited to testis/scrotum
Spread to regional lymph nodes
Visceral or supra-diaphragmatic spread, OR regional node limited
disease with significant tumor marker elevations
Determine seminoma vs. non-seminomatous germ cell
tumor, then stage
**If AFP is elevated, even if histology looks like
seminoma, its a NSGCT!
Extremely sensitive to chemo and radiation! Will kill all of
tumor! Always orchiectomy, then: Stage I = 1 dose of chemo;
Stage II = radiation; Stage III = course of chemo
Non-seminomatous germ cell tumor = sensitive to chemo,
but may have teratomatous elements that remain after
chemo that have to be surgically removed
Stage I orchiectomy + observation. Stage II/III = chemo
surgery to remove residual masses.
1.
Terminolog
y
Pathophysi
ology
Evaluation
Manifestati
ons
Pathology
Treatment
Clinical BPH
Microscopic
BPH
Macroscopic
BPH
Lower UT
symptoms
(LUTS)
Overview
Lower urinary tract symptoms (LUTS), bladder dysfunction, hematuria, UTI resulting from
macroscopic BPH
Histologic evidence of cellular proliferation of the prostate
Enlargement of the prostate resulting from microscopic BPH
Complex of voiding symptoms (straining, hesitancy, urgency, frequency) that may be caused
by macroscopic BPH
Proliferative process of stromal and epithelial elements of the prostate -> macroscopically
enlarged prostate gland
Originates in transition zone around urethra; typically in men >40. Unknown etiology. Not
pre-malignant!
History
Identify other causes of voiding dysfunction
Digital Rectal
Check prostate size. Does not correlate precisely with symptom severity, degree of
Exam
obstruction, or treatment outcomes
Urinalysis
R/o UTI, hematuria
Serum PSA
If detection of prostate cancer would alter management (not super old)
Other
Uroflow, postvoid residual, urodynamics, transrectal ultrasound
LUTS, poor bladder emptying, urinary retention, overactive bladder, UTI, hematuria, renal insufficiency
Gross
Microscopic
Behavioral
Medical
Surgery
Enlarged, nodular prostate. Discrete periurethral nodules, may compress prostatic urethra
Both stromal and glandular proliferation. Mixed hyperplasia + hypertrophy. Drive by T->
5R -> DHT
fluid intake, avoid caffeine/EtOH, timed voiding
-blockers (tamulosin): block 1-ARs in prostate -> relax prostatic smooth muscles ->
bladder outlet obstruction; get improvement in sxs and flow rate
5--reductase inhibitors (Finasteride, Dutasteride): block conversion of T -> DHT via
competitive inhibition -> prostate size by up to 50%; sxs and risk of surgical
intervention, urinary retention
--Side effects: libido, ejaculatory disorder, impotence, breast enlargement
Anticholinergic medications: block cholinergic receptors in the bladder that enable bladder
contractility; for men with overactive bladder associated with chronic outlet obstruction
outlet resistance: trans-urethral resection of prostate, laser prostatectomy, simple
prostatectomy
2.
Explain how medical interventions for symptomatic benign prostatic enlargement impact the pathophysiology of
the condition.
3. Discuss benign versus malignant causes of elevated serum PSA.
Prostate Specific Antigen
Description Serine protease responsible for semen liquefaction, specific to prostate. A marker of risk with imperfect sensitivity
and specificity
Elevation
Disruption of cellular architecture - prostate cancer, prostatitis, BPH, prostate massage, prostate biopsy
Normal
with age and prostate size, no normal value, just a range
PSA
4.
Discuss the pathophysiology of prostate cancer, and compare the natural history of low risk and high risk disease.
Prostate Cancer
Epidemiology
Common condition associated with aging; 75% of men >85 years! Most common non-skin cancer in US men.
Lifetime risk of disease = 16.7%, lifetime risk of death = 2.6%. Incidence with screening.
Etiology
Multifactorial androgens, age, race (AfAmerican), family history of early cancer, inflammation,
environmental + genetic influences
Detection
PSA: discussed above
DRE: assess size, nodules, + confounders of elevated PSA (like prostatitis)
Prostate biopsy: transrectal, US guided; take 12 biopsies of peripheral zone
Risk
Low risk: PSA < 10, Gleason 6, cT1c-2a. High cure rate, but most would never have caused problems!
Categories
Takes 15-20yrs to cause issues. Treat very low risk dz with active surveillance
Intermediate risk: PSA 10 but <20, Gleason 7, cT2b
High risk: PSA 20, Gleason 8-10, cT2c+; often metastasize by time of diagnosis
-- risk of progression and mets without treatment, also recurrence and mortality with treatment
Determined by highest of any one score (i.e. if PSA20, always high risk)
Gross
Tough to see (chalky yellow), need to sample entire gland
Pathology
Histology
Cells larger than normal, ampiphilic, prominent nucleoli
Gleason
Based on gland architecture. Cytologic features similar in all grades. Starts at grade 3 (nodule with small
Grading
infiltrating tubules), then up to grade 5 (no gland formation, just solid sheets with necrosis)
System
Gleason Score = primary grade (most prevalent grade recognized) + secondary grade (second most
prevalent grade recognized)
Pathologic
pT1: clinically unapparent tumor, incidental
Stage
Select Biopsy
Findings
Progression +
Symptoms
Treatment of
Metastatic
Disease
1.
2.
3.
4.
5.
6.
7.
8.
Uteru
s
Normal
Polyps
Endometrial
Cancer
Fibroids
Ovari
es
Normal
Simple Cyst
Hemorrhagic
Cyst
Endometrioma
Torsion
Tubo-ovarian
Abscess
Tumors
Ectopic
pregnancy
Teste
s
Prost
ate
Normal
Torsion
Epididymo-Orchitis
Tumors
Varicocele
Normal
Cancer
Distends endometrial cavity. Cervix is cannulated and contrast dye is injected into
Terms are density, attenuation
Terms are signal intensity, brightness
Uses very high frequency sound waves that reflect to form an image. Terms are an/iso/hyper/hypoechoic.
Passes straight through fluid (anechoic), completely reflected by calcium and air. Can use Doppler to
see flow
Sonohysterogram: fluid injected into endometrial cavity, outlines mucosa
Ante- or retroverted, homogeneous myometrium. Echogenic endometrium, varies in appearance with
age and phase of menstrual cycle. Early proliferative = line, secretory = big white gob. Mid-cycle = 3
nice layers (trilaminar phase)
Growths into cavity from mucosal/glandular surface. Echogenic (bright) mass with vascular pedicle
Abnormally thickened endometrium with possible invasion of myometrium. Heterogeneous,
disorganized, very vascular.
Fibrous smooth muscle growths that come from myometrium. Can be submucosal (most problematic),
intramural, or subserosal. Darker than surrounding myometrium. Can be calcified
Attached to broad ligament, anterior to iliac vessels.
Contains small follicles, dominant follicle, or corpus luteum (huge) depending on phase of cycle
Thin walled, purely anechoic structure (filled with serous fluid). Color Doppler is key!
Complex, heterogeneous cyst with blood (less black than serous fluid). Flow only around edge. May
have clot or fibrin stranding.
Homogeneous adnexal cyst filled with old blood products
Enlarged, edematous, abnormal looking ovary w/ /no blood flow (loses venous drainage). Check
for lead point (causes twisting)
Complex mass in adnexa. Usually from ascending infection -> PID
Complex cystic or solid ovarian lesions. May be asymptomatic until large
Usually b/t uterus and ovary in fallopian tube. Complex adnexal mass w/ echogenic vascular ring of
blood flow. Must do pregnancy test! Dont definitively call pregnancy intrauterine until you
see yolk sac!
Homogenous testes + epididymis, with symmetric vascularity
/absent blood flow
blood flow in testes and epididymis due to infection and inflammation
Focal mass. Often hypoechoic.
Enlarged tortuous veins, commonly on left side (left gonadal vein -> left renal vein rather than IVC)
Transitional zone hypoechoic relative to more echogenic peripheral zone
Mass on US
Spermat
ogenesi
s
Evaluati
on of
Infertile
Male
Treatme
nts
Cell
types
History
Fertility
Preserv
ation
Never forget you are a doctor first, no matter what specialty you practice
For both male and female:
o Be healthy:
Balanced diet
Exercise
Sleep
Anatomy
Physiolog
y
Mechanis
m of
Tumescen
ce
Erectile
Dysfuncti
on
Basic
Workup
of ED
Treatment
Options
Penis
Priapism
Most ED is vasculogenic
Treatment begins with oral agents
o PDE5 inhibitors
o Increase intracellular cGMP
o Increase in intracavernosal sm. muscle relaxation
Priapism
o High flow
o Low flow