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Repro > Week 3 > Flashcards

Week 3 Flashcards

1
Q

veinous drainage vs lymphatic drainage from breast

A

veinous mostly medial, lymphatic mostly axillary

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2
Q

alveolar epithelial cells

A

form lobule membranes in TDLUs

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3
Q

myoepithelial cells

A

smooth muscle component surrounding epithelial cells of duct to help expel milk

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4
Q

hormonal requirements of breast development

A

-pre-puberty: no sexual dimorphism! Ducts extend short distance into stromal fat pad
-Puberty (ductal morphogenesis): Estrogen. Requires normal pituitary function
-Pregnancy (lobuloalveolar development): Progesterone/Prolactin
Lactation: Prolactin, (cortisol/insulin)

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5
Q

Fetal Development of breast

A

hormone-independent: Milk streak–> mammary bud –> primordial ductal tree

Hormone-dependent events (placental sex steroids): canalization of ducts, parenchymal differentiation and colostrum formation

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6
Q

time at which mitotic rate of breast is greatest

A

luteal phase (E2 + P is more mitogenic than E2 alone)

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7
Q

Breast in pregnancy

A

Dramatic changes in hormones.

Progesterone, prolactin –> proliferation and differentiation of lobuloalveolar cells

Progesterones and Estrogens inhibit lactogenic action of prolactin

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8
Q

lactation control

A

loss of placenta –> drop in E2 and P. unopposed prolactin –> final differentiation of alveolar cells.

  • projection/ejection controlled by neural reflex arcs (ending in oxytocin –> myoepithelial contraction)
  • suckling –> more prolactin –> more milk production
    needs: intact HPA, regular removal of milk, nutrition (not ovaries!).
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9
Q

postlactational involution

A

increased pressure in acini –> permanent changes in breast (apoptosis of 80% of epithelial cells)

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10
Q

galactorrhea

A

associated with hyperprolactinemia, amenorrhea

or increased sensitivity of breast to prolactin

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11
Q

Sheehan’s Syndrome

A

infarction of pituitary during L/D

lack of post-pardum lactation can be first sign

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12
Q

Gynecomastia cause

A

decreased Androgen : Estrogen ratio!

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13
Q

endocrine risk of breast cancer

A

exposure to estrogen (age at menarche, menopause etc)

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14
Q

BRCA1 in men

A

mildly increased risk of breast, pancreatic, prostate (?) cancer. so can be hidden in family Hx in families with lots of men.

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15
Q

BRCA2 in men

A

increased risk of melanoma, prostate cancer, etc (tend to be worse cancers)

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16
Q

Who to refer for genetic testing?

A

Breast and ovarian cancer in single lineage. Breast cancer 2 women in a single lineage with cancer <50 yo

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17
Q

cardinal rule for genetic testing

A

Test the affected individual first(!)

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18
Q

management of breast cancer risk in BRCA1/2 carriers

A

annual mammogram and MRI >25, monthly SBE, biannual CBE, oophorectomy, SERM chemoprevention, mastectomy.
-RRSO

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19
Q

Management of ovarian cancer risk in BRCA1/2 carriers

A
  • risk reducing salpingo-oopherectomy (RRSO) by 35-45 once child bearing complete
  • screening until then
  • OCP
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20
Q

BRCA1 vs BRCA2

A

BRCA2 tends to be ER+, BRCA1 tends to be triple neg

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21
Q

Treatment of BRCA1/2 cancers vs others

A

No difference in prognosis! May change type of chemotherapy (cisplatin?)…early data that respond well to PARP inhibitors (knocks out parallel DNA repair pathway and leads to cytotoxicity)

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22
Q

“tell me about yourself in the future” study of LGBT youth

A

foreshortened sense of future, on average less thinking about mid-life events. Effect on choice-making and risky behavior.

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23
Q

Mechanism for health disparities of LGBT adults

A

“internalized homophobia” stress etc. Barriers to health care (benefits, bias, visitation rights, legacy of distrust.)

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24
Q

Suicide predictors for LGBT youth

A

male, closeted, period after self-labeling, feminine gender role concept, drugs and alcohol

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25
Q

suicide mitigators in LGBT youth

A

greater proportion of same-sex couples, GSA, LGBT non-discrimination policy in school etc

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26
Q

LGBT health disparities

A

substance use, stress (cortisol), suicide, depression and anxiety, domestic violence (rate is the same, but screening is less.)

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27
Q

impact of same-sex marriage on health

A

states with bans on same-sex marriage increase mood disorder, substance use, etc.

states with legalized marriage have positive effect (not a ton of data)

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28
Q

risk of cancer in lesbians

A

ovarian, cervical, and breast cancer:
fewer pregnancies, increased BMI, increased alcohol use, reduced screening!! (physician and patient factors)
no screening should be different!!

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29
Q

health risks in gay men

A

anal: related to exposure to HPV, not related to top/bottom
eating disorders
STIs and HIV, HIV-associated cancers (increased in adolescent LGBT minorities)

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30
Q

transgender health disparities

A

higher rates of substance abuse and victimization, prostitution and sex trade, “street hormones”

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31
Q

classification of mullerian anomalies

A

vertical fusion defects, horizontal fusion defects (doesn’t affect ovaries!)

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32
Q

vertical fusion defects

A

vaginal septa
imperforate hymen (technically urogenital abnormality)
Cervical agenesis/dysgenesis
Mullerian agenesis (MRKH)

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33
Q

lateral fusion defects

A 
uterus didelphys two hemi-uteri and cervices 
bicornuate uterus
septate uterus
unicornuate uterus
obstructed defects
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34
Q

lateral fusion defect association

A

renal abnormalities: renal agenesis ipsilaterally

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35
Q

loss of uterus/vagina DDx and Tx

A 
mullerian agenesis (MRKH)
androgen insensitivity
Tx:
form vagina (pressure technique 90% successful, surgical management possible but not favored by gynecologists). MRKH individuals can have children via surrogate.
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36
Q

8 risk factors for breast cancer

A

sex, age (>50), geogrpahy, family Hx, fibrocystic changes (some), prior breast or gyn cancer, radiation, estrogen exposure

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37
Q

properties of carcinoma in situ

A

microscropic, “in position” proliferation (confined by basement membrane), lacks ability to spread, benign-acting

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38
Q

histologic appearance of DCIS

A 
obliteration of normal epithelium by carcinoma cells 
enlarged cells
high N:C ratio
prominent nucleoli
increased mitoses
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39
Q

properties of DCIS

A

most common form of BC
lacks capacity to spread
always curable, if treated
non-obligate precursor to invasive cancer!
appears as cluster of calcifications on screening mammogram

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40
Q

two types of calcification

A

dystrophic (necrosis)

metastatic (hypercalcemia)

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41
Q

acini

A

lobules of breast

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42
Q

features of LCIS

A

microscopic
proliferate “in position” (confined by basement membrane)
generally incidental finding (doesn’t generate calcifications)
benign, difficult to excise
risk factor or precursor?
Tx: Watch and wait +/- tamoxifen (if ER+)

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43
Q

path of LCIS

A

features of carcinoma
lack of cohesion
signet rings

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44
Q

features of invasive breast cancer

A

no longer in situ
capacity to spread
potentially lethal
10 yr survival ~50%

45
Q

paget disease

A

crusting and ulceration of nipple occurs when breast carcinoma cells migrate into squamous epithelium of epidermis
can be seen with DCIS or invasive ductal carcinoma

46
Q

“inflammatory” breast carcinoma

A 
type of ductal
reddened skin
\+/- mass
evolves rapidly
invasive, virulent
uncommon
47
Q

invasive lobule carcinoma

A

grows in linear infiltration pattern (boxcar formation)

48
Q

Breast cancer staging

A 
TNM
Tumor size (Tis, T1, T2, T3 (cm))
Lymph nodes (N): N0, 1, 2, 3
Metastasis (M): M0, 1, x
Stages: 0 (in situ), - 4
49
Q

predictive markers in breast cancer

A

ER, PR, Her-2/neu

50
Q

Molecular profiling in breast cancer

A

limited use
Oncotype DX used for N0, ER+, can handle Tamoxifan 5yrs…yields recurrence score
low-risk: gain from chemo outweighs risk (just tamoxifen)
high-risk: use chemo + tamoxifen

51
Q

Breast carcinoma in Men

A

uncommon
Klinefelter Syndrome (XXY)
ductal only
staging, treatment, and outcome same as for women

52
Q

Fibrocystic changes (epi, etiology, Sx, significance, classification)

A
  • common, reproductive years
  • hormonal etiology?
  • benign
  • cyclic pain, tenderness, palapble mass, -abnormal mammogram (mass or calcifications)
  • importance: is it cancer? some are risk markers
  • proliferative vs non
53
Q

non-proliferative fibrocystic changes

A

fibroses, cysts, adenosis (increased # acini), apocrine metaplasia (convergence of glands)

54
Q

proliferative fibrocystic changes

A

sclerosing adenosis (fibrosis and icnreased # acini. compression/distortion of glands)
Usual Duct hyperplasia
Atypical Duct hyperplasia
Atypical lobular hyperplasia (atypicals have some characteristics of CISs, but not quite)

55
Q

increased risk of breast cancer with benign breast disease

A

slight: sclerosing adenosis, moderate usual ductal hyperplasia, florid ductal hyperplasia
moderate: atypical hyperplasias
high: atypical + family Hx of breast cancer

56
Q

big picture of biopsy

A

most biopsies reveal benign conditions that don’t carry increased risk.
most cancers arise in women who don’t get biopsies

57
Q

benign tumors of breast

A

fibroepithelial: fibroadenoma, phyllodes tumor
epithelial: intraductal papilloma

58
Q

fibroadinoma

A 
most common benign tumor
reproductive years
solitary, multiple, or bilateral 
excision is always curative (not necessary!)
no excess cancer risk
Always circumscribed
59
Q

phyllodes tumor

A 
uncommon
reproductive years
solitary
excision almost always curative
no excess cancer risk
invasive border, high cell density
60
Q

intraductal papilloma

A

Large duct lesion (uncommon)
nipple discharge, bleeding
completely benign
no increased risk

61
Q

inflammation of breast

A

infectious: post-partum (S aureus, strep)
non-infectious: “traumatic” fat necrosis (temporarily related to trauma, after resolution yields hard mass, calcification, granulomatous inflammation)

62
Q

gynecomastia

A

breast enlargement
common in men
adolescents (will often resolve on its own) and elderly
relative estrogen excess –> ductal proliferation and myofibroblast proliferation
NO increase in cancer risk (except in XXY)
bilateral or unilateral

63
Q

Normal male breast

A

ducts, no lobules. Largely fat and connective tissue

64
Q

key steps in early placental development

A

Differentiation of trophoblast from OCM
implantation of blastocyst
development of lacunae in tropho plaque (–> intravillous space)
Invasion of cytotrophoblast cords to form primary villi
ingrowth of vasculogenic villous stroma to form secondary villi
formation of villous capillairies (tertiary villi)

65
Q

spontaneous abortion

A

pregnancy loss <20 weeks gestation

~15% pregnancies

66
Q

abnormal implantation

A

ectopic pregnancy
90% in fallopian tube
predisposition with PID, scarring, surgery,

67
Q

structure of placenta

A

cord, placental disc (vessels), membranes

68
Q

umbilical cord

A

2 arteries, 1 vein, Wharton’s jelly (shock absorber)

usually central to placental disc

69
Q

placental membranes

A 
amnion (simple cuboidal epithelium), chorion, decidua
translucent
smooth texture
peripheral connection to placental disc
regulatory inflammatory cells
70
Q

classification of multiple gestation

A 
# of chorions, # of amnions 
dichorionic could be mono- or di-zigous
71
Q

two pathways for placental infection

A
  • ascending via birth canal (more common, usually bacteria, can cause sepsis/meningitis in baby, frequent cause of preterm). Chorioamnionitis.
  • hematogenous (viral–CMV, toxo, syphilis, rarely bacteria if sepsis. Can cause growth restriction, fetal demise. Causes placental inflammation–villitis)
72
Q

inflamm response to placental infection

A

maternal PMNs. Fetal if severe. Fetal response associated with long-term sequelae

73
Q

vascular lesions of placenta

A
  • lesions disrupting flow between uterus and placenta or between placenta and fetus (torsion, knots of cord)
  • clinical impact depends on the size, location, nature of lesion
74
Q

retroplacental hemorrhage (Sx, risk factors, path)

A
  • maternal pain, bleeding, uterine enlargement.
  • risk: HTN, increased age/parity, preeclampsia, smoking, thrombophilia, cocaine)
  • path: acute villous infarction

Pathological correlate for “abruption” (clinical term)

75
Q

preeclampsia (clinical, epi, consequences, etiology, path

A
  • Maternal HTN, proteinuria, edema
  • 3% pregnancies
  • high morbidity/mortality for mother and fetus if not managed
  • superficial implantation of the placenta. incomplete remodeling of uterine spiral arteries by cytotrophoblast invasion (reduced flow)
  • path: atherosis of spiral arteries. fibrinoid necrosis and lipid-laden macrophages.
76
Q

chorangioma

A

proliferation of capillaries and stroma. Benign, only cause trouble when very large or occlude cord

77
Q

molar pregnancy

A

-complete: completely paternally derived (1 or 2 sperm fertilize empty ovum). diploid. lack fetal parts and characterized by trophoblast hyperplasia and edema. lower risk of trophoblast tumors
-partial: mixed maternal/paternal derivation. 2 sperm fertilize normal ovum. triploid. fetal parts + variable/focal trophoblast hyperplasia and stromal edema. lower risk of trophoblast tumors.
Clinically: will manifest of pregnancy Sx with abnormally high hCG

78
Q

45, X Syndrome

A

most common chromosomal abnormality in early pregnancy. detected prenatally with cystic hygroma +/- hydrops. can survive to birth: small stature, horseshoe kidney, bicuspid aortic valve, mullerian abnormality

79
Q

TORCH infection

A

Toxo, Other (syphilis, Parvo), Rubella, CMV, Herpes

Fetus ~ immunocompromised

80
Q

complications of prematurity

A
  • hyaline membrane disease and chronic neonatal lung disease
  • necrotizing enterocolitis
  • intraventricular hemorrhage
  • sepsis
  • long term complications (inc developmental delay)
81
Q

hyaline membrane disease

A 
most common cause of respiratory distress in newborns.
decreased area and decreased surfactant
-->ground-glass radiology
hypoxemia.
Tx: exogenous surfactant
82
Q

germinal matrix

A

transient structure comprised of glial and neuronal cells with dense venous network. decreases 16-34 weeks. can hemorrhage in premature infants

83
Q

congenital hemangiomas

A

most common neonatal tumor. benign but location matters

84
Q

respiratory changes in pregnancy

A
  • mechanical: chest circumference expands. diaphragm rises
  • URT: hyperemia, edema induced by estrogen, epistaxis
  • reserve volume decreases, tidal increases, minute volume increases 40% (blow off CO2 from fetus, more susceptible to resp disease)
85
Q

cardiac changes in pregnancy

A
  • cardiac output increases 30-50%. Term uterus gets 17% of C.O.
  • Heart bigger on CXR, rotated toward the chest wall, more horizontal
  • progesterone –> drop in systemic arterial pressure (prevents HTN).
  • systolic ejection murmors 90%. Diastolic murmurs not normal.
86
Q

hematologic changes in pregnancy

A
  • increase in blood volume, decrease Na+ osmolarity
  • vol increases 40-50%, RBC by 18-30% –> physiologic anemia of pregnancy
  • other causes of anemia must be evaluated
  • hypercoaguable –> 2X risk in thromboembolism. even higher postpartum
  • bleeding and clotting times should not change in pregnancy. increased fibrinogen, factors I, VII, VIII, IX, and X
87
Q

renal changes in pregnancy

A

-hypertrophy, dilation of ureters…UTIs and kidney infection. due to progesterone!

88
Q

GI changes in pregnancy

A

progesterone –> smooth muscle relaxation.
-decreased emptying time, acid reflux, sphyncter weakness, predisposition to gallstones
estrogen –> liver increases production of clotting factors
hCG –> nausea and vomiting

89
Q

Three P’s

A

Passenger: presentation, size, position
Passage: inlet, midplane, outlet. Zero-station: leading edge of head has reached mid-plain.
Power: contractions. maternal effort

90
Q

labor (def, cause)

A

regular uterine contractions leading to cervical dilation.
Cause: not known exactly. prostaglandins, intracellular Ca, oxytocin; collagenase/elastase in cervix
Gap junctions allow myometrium to contract simultaneously.

91
Q

labor stages

A

1: closed - fully dilated (latent, active)
2: fully dilated - delivery
3: placenta

92
Q

cardinal movements

A 
engagements ("0 station)
flexion and descent
internal rotation, further descent
compete extension
corrective external rotation
deliver anterior shoulder
deliver posterior shoulder
93
Q

cardio postpartum

A

immediate postpartum period is most dangerous

increased SV will persist for 1-2 weeks

94
Q

vaginal lacerations

A

1st: vaginal mucosa
2nd: subcutaneous tissue
3rd: anal sphincter
4th: rectal mucosa

95
Q

placental ecreta

A

abnormal adherence of placenta. can result in excess bleeding, may need to do C-hysterectomy

96
Q

Shoulder Dystocia

A

ant shoulder stuck behind pubic symphysis (can result in brachial plexus injury

97
Q

Fetal HR monitoring

A

Doppler-based
Uterine contractions, baseline rate, FHR variability, accelerations/decelerations, trend over time
Cat I: normal
Cat III: abnormal. need to deliver
Cat II: indeterminite.
FHR should increase with contraction (reduced blood flow)

98
Q

indications for c-sections

A 
prior c-section
abnormal labor
cephalopelvic disproportion
congenital anomalies
multiple gestations
worrisome heart tones
previa
fetal malpresentation
elective
99
Q

types of trophoblasts

A

invasive (extravillous)

villous (cyto- and syncytio-) exchange nutrients and secrete hormones

100
Q

adaptive pressure on fetal circulatory system

A

lower PO2 than adults (max is that of uterine artery)

101
Q

Adaptations of fetal circulatory system to lower oxygen content of uterine artery

A
  • Fetal Hb
  • elevated heart rate (~160 bpm)
  • circulatory ducts maximized oxygen to brain and coronary arteries: 1) ductus venosus shunts blood to vena cava 2) foramen ovale: blood from IVC goes into right atrium and mixes with blood from SVC, but dominant current is to left atrium –> brain 3) ductus arteriosus bypasses lungs from circulation
102
Q

trophoblast functions

A
  • hormone production (syncytio primarily)
  • nutrient transport
  • express HLA-G to prevent immune rejection (prevents NK killing and not recognized as non-self)
103
Q

hCG

A
  • secreted by syncytiotrophoblasts.
  • same alpha subunit as LH, FSH, TSH
  • binds LH/CG receptor
  • targets ovary to maintain progesterone production (weak thyrotrophic activity)
  • doubles ever ~2 days, peak at 10 days
104
Q

prenatal genetic testing

A

some peripheral proteins can be tested for. levels correlate with down syndrome. Can also do CVS and amniocentesis, now can isolate free fetal DNA in peripheral blood

105
Q

feto-placental steroid synthesis

A
  • fetal adrenal lacks most enzymes, pours out DHEA (not making cortisol so no negative feedback. Placenta has enzyme that deactivates maternal cortisol–important! can use steroids in pregnant women)
  • placental can make progesterone, also can take fetal DHEA and make estradiol
106
Q

actions of progesterone

A
  • smooth muscle relaxant: allows uterus to expand but causes “side-effects” of pregnancy (UTIs, constipation, GERD)
  • prepares endometrium for implantation during luteal phase
  • prevents immune rejection of fetus by suppressing cytokines
107
Q

initiation of parturition

A

late in pregnancy, uterus loses responsiveness to progesterone (by switching receptor subtype)…less relaxed, starts contracting

108
Q

actions of placental estrogen

A
  • not well understood
  • vasodilation of spiral arteries
  • parturition: stimulates placental production of CRH, myometrial gap junctions, mammary epithelial cell proliferation in preparation for milk production

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