Breast + OB/GYN Flashcards Preview

CPP3 > Breast + OB/GYN > Flashcards

Flashcards in Breast + OB/GYN Deck (40):

Types of benign breast disease

Fibrocystic change (lumpy bumpy, young women)
Fibroadenoma (well circumscribed, mobile mass)


Risk factors for breast cancer

Cumulative lifetime estrogen/progest exposure
Famiily hx/genetics (Caucasians, BRCA1/2)


Screening mammogram frequency
Worrisome features
Follow up

- q2 ages 50-69
- spiculated, irregular borders
- Follow up abnormal mammo or palpated breast mass with diagnostic mammogram/US and if still concerning, with core biopsy (preferred), FNA in some cases. Maybe MRI
- Surgery +/- chemo +/- radiation +/- antiestrogen meds


Types of Breast Carcinoma
- Histology (2)
- precursor, subtypes, prognosis, trx
- Receptor status

1) Invasive Ductal Carcinoma (80%)
- Precursor = DCIS
- Subtypes: a) Tubular (good); b) Mucinous (good, older women); c) Medullary (good, BRCA1, OK); d) Inflammatory (poor)
2) Invasive Lobular Carcinoma (20%)
- Precursor (optional) = LCIS (tamixofen = anti-estrogen)
- Mutation in E-cadherin; single-file pattern, signet cells, no duct formation

- Receptor status
1) ER/PR (most cancers, good prognosis, hormone therapy = tamoxifen)
2) HER2/Neu (poor prognosis, but positive predictive factor bc responds well to trastuzumab = Ab against HER2 receptor)


Breast cancer trx

1) Surgery: partial mastectomy, lumpectomy + sentinel node dissection, full axillary node dissection if sample nodes positve
2) Radiation: required after lumpectomy to be as good as partial mastectomy
3) Chemo: when high risk for or known distant dz
4) Receptor target therapy:
ER/PR+: tamoxifen (pre-menopausal), anastrazole (post meno, aromatase inhibitor)
Her2+: trastuzumab (Herceptin)


DDx for abnormal uterine bleeding

- Polyps (= abnormal bleeding between periods)
- Adenomyosis = endometrial tissue in myometrium (painful periods, bulky and globular uterus)
- Leiomyoma = benign smooth mm tumor (heavy periods, pelvic pressure, shrink after menopause)
- Malignancy/Hyperplasia

- Ovulatory dysfn
- Endometrial
- Iatrogenic
- Not classified


Leiomyoma trx

Meds: NSAIDs, OCP, GnRH agonist (leuprolide), transexamic acid
Sx: uterine aa embolization, myomectomy, hysterectomy


Carcinomas of uterus/endometrium

1) Leiomyosarcoma (uterine smooth mm)
2) Endometrial adenocarcinoma
- Type 1 (endometrioid): most common, hyperplasia ==> carcinoma, PTEN mutation
- Type 2 (non-endometrioid, serous or clear cell), atrophic endometrium => carcinoma, p53 mutation


Endometrial hyperplasia
- Results from
- Risk factors
- Hereditary syndrome associations
- Risk of progession to cancer and how to trx

- Results from unopposed excess estrogen leading to endometrial lining buildup
- RFs: obestiy, early menarche/late menopause, anovulation (eg PCOS), exogenous estrogen, estrogen-producing tumors
- Lynch (nonpolyposis colorectal cancer) and Cowden (PTEN mutation) syndromes

- Simple hyperplasia w/o atypia: "penny" = 1%; progestins 2wks/month or IUD
- Complex hyperplasia with atypia: "nickel" = 3%; continuous progestins or IUD
- Simple hyperplasia with atypia: "dime" = 9%; D&C to rule out adenocarcinoma then progestins/IUD
- Complex hyperplasia with atypia: "quarter" = 27%; hysterectomy


Goal of pap smear screening

ID pts with dysplasia likely to progress to cancer (HSIL/CIN II or III) without performing unnecessary procedures on those unlikely to progress (LSIL/CIN I)


HPV infects where?
Low and High risk types

Transformation zone of cervix
- Low: 6, 11 --> self resolve
- High: 16, 18, 31, 33 --> may progress to cancer


Pap smear screening guidelines
- < 21
- 21 - 29
- 30- 65/70
- 65/70+

1) No pap, don't do HPV, if done ignore results

2) q3, do HPV if get ASC-US, yearly if high risk (= hx of CIN 2, 3; HIV infxn or immunocompromised)

3) q5, yes HPV, screen more freq if high risk

4) stop paps after 3 consecutive negative paps and no hx of CIN 2,3 but screen annually for high risk


Dysplasia mgmt (Result, qualifiers, f/u)
- Normal
- ASC- US (atypical cells of undet significance)
- ASC-H (Atypical cells can't rule out high grade)

1) Normal: f/u every 1-3 yrs

2) ASC-US: significant only if HPV + --> colposcopy

3) ASC-H: probably CIN 2,3 --> colposcopy

4) LGSIL/CIN1: HPV presumed --> colposcopy

5) HGSIL/CIN2,3: HPV presumed --> colposcopy, may go straight to excision (LEEP)


Diagnosis and dating of pregnancy
- Day 1
- Day 8
- Day 14

- D1: fertilization
- D8: implantation, hCG secreted by blastocyst detectable in serum
- D14: hCG detectable in urine


What does hCG do?

- hCG keeps corpus luteum (produces progest) from degenerating until placenta takes over production at 7-9 weeks
- Useful marker of normally developing pregnancy/detecting abnormal; should double every 48h until plateau in wks 11-12


How to date pregnancy/delivery

40 weeks from LMP or LMP - 3 months + 7 days
Use 1st trimester crown length if LMP unknown


Process of implantation
- If trophoblasts don't completely penetrate...

- Syncytiotrophoblasts invade decidualized endometrium forming chorionic villi
- Vascular remodeling of spiral aa --> replacement of smooth mm so they are resistant to vasoactive substances and dilated low-pressure systems
- If incomplete penetration, smooth mm not completely replaced so you have a high pressure system with less blood flow --> possibly pre-eclampsia


Hormones during early pregnancy and effects

- Progesterone: maintains endometrium, inhibits immunity, prevents contraction
- Human Placental Lactogen: increases insulin resistance via IGF-1, favors lipolysis, gluconeogensis, and glucose to fetus --> contriubtes to gestational diabetes


Maternal physiology changes
- Cardio/Heme
- Pulm
- Renal
- GI
- Breast
- Skin/Teeth/Hair

- Cardio/Heme: increase CO 30-50% (1/2 SV goes to fetus); increase plasma volume more than red cells --> anemia; plts down, WBC up --> prothrombotic
- Pulm: TV and MV up --> respiratory alkalosis and dyspnea; O2 consumption up; FRC and RV down bc no room
- Renal: GFR up and more flow, UTIs, risk for pyelo
- GI: progesterone loosens sphincters --> constpiation
- Breast: estrogen --> ducts, progesterone --> alveola
- S/t/h: stretch marks, hair stays in, palmar erythema, gum bleeding


Stages of labor

Labor = uterine contraction that produces cervical change until 10 cm
Stage 1: Dilation (<4cm latent, up to 10cm active)
Stage 2: 10 cm to delivery
Stage 3: baby to placenta delivery


Activation of mat/fet HPA axis

Fetus cortisol --> dec progest binding --> inc CRH production --> inc prostaglandins --> uterine contractions, more oxytocin, more CRH release


- What stimulates colostrum during pregnancy?
- Role of progesterone
- Galactopoiesis: hormones and stimulation

- hPL, prolactin, and hCG stimulate colostrum during pregnancy
- Progest suppresses prolactin until delivery when it falls and high prolactin stims milk to come in
- Galactopoiesis: suckling, prolactin from AP stims milk let down, oxytocin from PP stims ejection via myoepithelial cells lining breast alveoli


Pre-eclampsia definition
- severe features

- HTN (> 140/90) + proteinuria (0.3g/24h or 0.3 P/Cr ratio after 20 weeks gestation
- Severe: BP >160/110, thrombocytopenia (<100k), renal insufficiency (Cr>1.1), impaired liver fn, pulm edema, visual/cerebral sx


Pre-eclampsia plus syndromes

- Eclampsia: preeclampsia + seizures
- H EL LP: preeclampsia + hemolysis + elevated liver enzymes + low plts


Management of pre-eclampsia depends on?
- Cornerstones

- Depends on gestational age and severity
- Cornerstones:
- Seizure prevention: Mg + monitor deep tendon reflexes which dec with Mg toxicity
- Control HTN: hydralazine, labetalol, nifedipine
- Delievery is the cure, but ideally manage until you can stim fetal lung development with betamethasone


- Types and why; risks

- Di/di (two placentas, two amniotic sacs), monozygous twins that split before day 3 or dizygous
- mono/di ( one placenta, two amnions), monozyg split days 3-9, twin-twin transfusion syndrome
- mono/mono (one placenta, one amnion), monozyg that split days 9-12, risk of tangling umbilical cords


Twin twin transfusion syndrome

With monochorionic-diamniotic twins. Abnormal placental vascular anastomosis results in one twin transfusing to other. Donor twin gets anemia, oligohydramnios, IUGR (small); recipient twin gets polycythemia, polydramnios, hydrops, high output cardiac failure


Pregnancy infections
- Types and can cause what
- Presentation

- Ascending: can cause chorioamnionitis (N.gonorrhea, bacterial vaginosis, Group B strep); may present as fever, uterine tenderness
- Hematogenous: can cause congenital malformations
- TORCH infxns: Toxoplasmosis, Other (Listeria, syphilis, VZV), Rubella, CMV, HIV/Hepatitis


Definition of infertility

1 year of unprotected sex without conception


Infertility causes and percentages

Male factor (dec sperm count, motility, etc.) (30%)
Ovulatory dysfn (20%)
Tubal/peritoneal (20%)
Uterine and cervical (5%)
Unexplained (25%)


Therapeutics uterine contractions
- Contraction requires rise in ___
- Which receptors lead to contraction and relaxation?

- Rise in intracellular Ca2+
- alpha1 receptors --> contraction
- beta2 receptors --> inhibit contract -->relaxation


Drugs that induce contraction and mechanism, SEs

- Oxytocin (pitocin): activate GPCR, inc Ca2+; SE=hypoTN, ADH effect, low urine output, pulm edema
- Prostaglandins E2 and F2alpha: vasoconstriction, promotes coordinated contraction


Medication for post partum hemorrhage



Drugs that stop contractions
- Why given?
- Mechs and SEs

To delay delivery until steroids can be given for lung development
- Magnesium sulfate: competes with Ca2+; SE: loss of deep tendon reflex, pulm edema, cardiac arrest, blurred vision
- B2 agonists (terbutaline): SE = pulm edema, hypoTN, tachycardia
- Ca channel blockers (nifedipine): SE = vasodilation and flushing
- Indomethacin (inhibits PG synthesis): SE = GI effects, premature closing of PDA


Drugs and pregnancy: categories and examples (C, D,X)

A: studies failed to demonstrate risk
B: animal studies show risk but not human studies OR no human studies but animal studies show no risk

C: Human studies lacking and animal studies show risk or lacking. Should only be given if benefit outweighs risk
- Quinolones, nifedipine, labetolol, fluoxitine, sumatriptan

D: studies show risk, but benefits to pregnant woman may be acceptable despite risk
- Coumadin, phenytoin, lithium, ACEs and ARBs (2nd/3rd tri)

X: Contraindicated
- Thalidomide, isotretinoin, valproate


Teratogens and effects

- Thalidomide: limb anomalies
- DES: clear cell carcinoma vagina, T-shaped uterus
- Antiepileptics: phenytoin (causes fetal hydrantoin syndrome); valproate (neural tube defects, depleted folate)
- SSRIs: paroxetine (cardiac problems 1st T, pulm htn in 3rd, fetal w/d)
- Benzos: cleft lip in 1st T
- Lithium: heart defect (Epstein's)
- ACEs: renal failure, oligohydramnios, skull hypoplasia


PCOS therapeutics

- Clomiphene citrate (anti-estrogen --> inc FSH and stimulates follicles)
- Metformin: insulin inc androgen levels from ovary, metformin dec androgen and induces ovulation
- Letrozole: aromatase inhibitor
- Oral contraceptives


Prolactinoma trx

Dopamine agonists: bromocriptine, cabergoline


IVF trx

1) Need oocytes so need FSH (recombinant FSH)
2) Need to prevent premature LH surge from so many follicles: leuprolide (GnRH agonist -- continuous GnRH = no pulsatile GnRH --> no FSH/LH --> gonads shut down)
3) Need LH for oocyte maturation (hCG)


Testicular tumors

1) Germ cell (95%)
- Seminomas (radiosenstive and better progn; peak in 30s)
2) Non-germ cell (usually Leydig cell tumors)
- Leydig cell tumors: testo secreting, can secrete estrogen; bimodal age range (kids and men in 30s); precocious puberty and gynecomastia; generally benign; Reinke crystals