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CMT > General Women's Health Patho > Flashcards

General Women's Health Patho Flashcards

1
Q

what are the lower genital cancers?

A

cervical, vaginal, vulvar

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2
Q

Menopause/Perimenopause

role of estrogen replacement pills

A
  • Vasomotor symptoms:hot flushes, night sweats →sleepdisturbances
  • Mood symptoms in perimenopause, but not postmenopause
  • GSM: vaginal dryness,dyspareunia

Routes of therapy:
* Systemic therapy: oral, transdermalpatches, topical gels
* Vaginal therapy: creams, vaginal tablets, ring
* Estrogen stimulatesendometrium→ progestin required if patient hasuterus

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3
Q

Menopause/Perimenopause

role of progestin replacement pills

A
  • Higher risk of adverse events thanestrogentherapy
  • Required for endometrial protection in patients withuterus
  • Selectionof route and dosing: Usually oral, Give cyclically if still menstruating regularly, Give continuously if post-menopausal
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4
Q

Menopause/Perimenopause

contraindications to HRT

A
  • Hormone-sensitivebreast cancer
  • High-riskendometrial cancer
  • Unexplained vaginal bleeding
  • Cardiovascular disease
  • Venous thromboembolism
  • Stroke ortransient ischemic attack(TIA)
  • Acute liver disease
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5
Q

Ovarian Torsion

anatomy of the ovaries

A
  • Also known as the female gonads
  • Paired intraperitoneal endocrine organ
  • Normal ovary is 2.0 cm in width, 3.5 cm in length and 1.0 cm in thickness
  • Mainly supported by the suspensory ligament of the ovary and the utero-ovarian ligament
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6
Q

Ovarian Torsion

functions of the ovaries

A
  • Hormone production: estrogen, testosterone, inhibin, and progesterone
  • Houses the oocytes, which begin developing in utero and pause development until puberty
  • At birth: 1-2 million oocytes
  • At puberty: 300,000 oocytes remain
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7
Q

Infertility

Female Fertility (timeline)

A
  • A woman’s peak reproductive years are between the late teens and late 20s
  • By age 30, fertility starts to decline; with decline happening faster once a woman reaches their mid-30s
  • By 45, fertility has declined so much that getting pregnant naturally is unlikely
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8
Q

Infertility

classifications of infertility

A
  • ovulatory dysfunction
  • tubal factors
  • uterine factors
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9
Q

Ectopic Pregnancy

ddx mnemonic

A

Non Gyn Causes
* H: hepatitis
* A: acute abd
* I: intestinal inflammation (appendicitis, diverticulitis)
* K: kidney stone
* U: UTI

GYN Causes
* P: PID
* O: Ovarian disorders (torsion, polycystic, cyst rupture)
* E: endometrial disorders (endometriosis, hyperplasia)
* M: miscarriage/spontaneous abortion

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10
Q

Cervical Cancer

pathway of dysplasia to cancer

A
  • Dysplasia: abnormal cells that have lost the ability to self regulate
  • PAP Smear/Liquid based cytology: Low Grade (LGSIL) c/w mild CIN 1; High Grade (HGSIL) c/w moderate to severe CIN 2-3
  • Cervical Intraepithelial Neoplasia (CIN) on biopsy - HOW MUCH OF THE CERVICAL EPITHELIUM IS INVOLVED (CIN 1 is mild, CIN 2 is mod, CIN 3 is severe)
  • Carcinoma in situ = “cancer in place” or cancer that has not spread beyond the epithelial layer
  • Invasive cancer= cancer has invaded tissue beyond the epithelial layer of cells

Can be ectocervical/endocervical

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11
Q

Cervical Cancer

subtotal vs total vs radical hysterectomy

A
  • Subtotal/partial hysterectomy: removal of uterus only, cervix remains
  • Simple/total hysterectomy: removal of uterus, cervix
  • Radical hysterectomy: removal of uterus, Fallopian tubes, cervix, bilateral parametrium and upper vagina
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12
Q

Placenta

Role of Placenta

A
  • Facilitating nutrient, and gas and waste exchange between maternal and fetal circulations
  • Serves as an endocrine organ producing hormones that regulate both maternal and fetal physiology during pregnancy
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13
Q

Placenta

what does the plaenta do early on?

A

Placental cells (trophoblasts) invade and start to remodel the uterine vasculature within a few hours after implantation → starts to produce hCG

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14
Q

Placenta

Structure

A
  • Flat, discoid organ measuring 20-25 cm in diameter and 3 cm in thickness
  • Membranes (fuses into a single membrane by delivery): Amnion (maternal) and Chorion (fetal)
  • Basal plate (maternal side):Divided into lobes, Separated by septa
  • Chorionic plate (fetal side):Contains branching chorionic villi, providing a massive surface for exchange, Umbilical cord emerges from the fetal side of the placenta
  • Umbilical cord: 2arteries (deoxygenated blood back to mom; away from baby’s heart), 1 vein (oxygenated blood to fetus)
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15
Q

Placenta

Placental Circulation

A
  • Chorionic villi provide a large surface area for maternal–fetal exchange
  • Spiralarteries(maternal) fill the intervillous spaces in the decidua basalis layer of the endometrium and bring in oxygenated blood for fetus
  • Spiralarteries“rupture” and become large spaces called lacunae
  • 2 umbilicalarteriesbring deoxygenated blood from fetus to placental chorionic villi
  • Gas and molecule exchange occurs between the fetal blood in the chorionic villi and the maternal blood in the lacunae, across the placental barrier
  • 1umbilical veintransports oxygenated blood back to the fetus
  • Maternalveinstake deoxygenated blood back to the maternalcirculation
  • Maternal and fetal blood never come into direct contact
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16
Q

Placenta

gas exchange role

A
  • O2-CO2exchange
  • Occurs via simplediffusion
  • Fetal hemoglobin has ↑ affinity for oxygen compared to maternal hemoglobin
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17
Q

Placenta

nutrient exchange (including waste product removal) role

A
  • provides materials needed for fetal development + growth
  • Water andsodiumby simplediffusion
  • Glucoseby facilitateddiffusion
  • Large molecules (LDLs, peptides,antibodies) by receptor-mediatedendocytosis
  • Amino acidsby secondaryactive transport
  • Waste Removal: products (urea and CO2) are transported back to the mother via simple diffusion
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18
Q

Placenta

define simple diffusion, facilitated diffusion, endocytosis, active transport

A
  • Simple diffusion is the process in which a substance moves through a semipermeable membrane or in a solution without any help from transport proteins
  • Facilitated diffusion isthe selective, passive movement of molecules along the concentration gradient
  • Endocytosis isa process in which a cell takes in materials from the outside by engulfing and fusing them with its plasma membrane
  • Active transport isthe process of moving molecules across a cellular membrane through the use of cellular energy; against a concentration gradient
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19
Q

Placenta

describe role in hormone secretion

which hormones?

A
  • Human chorionic gonadotropin(hCG): Maintains the activity of the corpus luteum required for continuation ofpregnancy
  • Human placental lactogen: Stimulates maternalinsulinproduction to ↑ glucose available to the fetus
  • Chorionic thyrotropin
  • Chorioniccorticotropin-releasing hormone(CRH)
  • Progesterone: Maintainspregnancy, preventsmenstruation
  • Estrogens
  • Glucocorticoids
  • Human growth hormone(hGH)
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20
Q

Placenta

name the 3 metabolic functions

A
  • Glycogen synthesis
  • Cholesterolsynthesis
  • Protein metabolism
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21
Q

Umbilical Cord

length

A
  • Extends from fetal umbilicus to fetal surface of placenta
  • Depends on amniotic fluid volume and fetal mobility
  • Average length: 55 cm
  • ≤ 40 cm is considered a short cord
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22
Q

Umbilical Cord

Structure of vessels

A
  • Contains 2arteriesand 1 vein
  • Vessels are surrounded by a protective substance called Wharton’s jelly
  • Counted by sonographic evaluation, with the 3 vessels seen in the 1st trimester
  • Coiling: the vein andarteriesspiral around each other
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23
Q

Umbilical Cord

blood flow

A
  • Umbilical vein supplies oxygenated blood to the fetus
  • Umbilicalarteriestake deoxygenated blood away from the fetus
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24
Q

Umbilical Cord

normal vs abnormal insertion into the placenta

A
  • NORMAL: central insertion
  • Eccentric: off center
  • Marginal: the cord inserts on the edge of the placenta
  • Velamentous: last portion of the umbilical cord lacks the protective Wharton’s jelly, leaving the umbilical vessels exposed
  • abnormal insertion increases the risk of complications during L&D (umbilical cord rupture or prenatal hemorrhage)
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25
Q

Amniotic Cavity

functions

A
  • Protects fetus against trauma
  • Protects umbilical cord against compression
  • Nutrientreservoirfor the fetus
  • Provides space for normal fetal growth and development
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26
Q

Amniotic Cavity

describe amnion + its functions

A
  • An avascular, tough but pliable membrane
  • 1 of the 2 primary fetal membranes
  • Ultimately fuses with the chorion
  • Functions of the amnion: Involved in solute and water transport required for amniotic fluidhomeostasis; Produces bioactive compounds
27
Q

Amniotic Cavity

Describe amniotic fluid + define normal volume, oligohydraminos, and polyhydraminos

A
  • Liquid that surrounds theembryoand fetus during its development
  • As the fetus grows, it “creates” amniotic fluid via urination, and continually “recycles” the fluid byswallowingit
  • Congenital defects inswallowingand/or the renal/urinary system can lead to abnormalities in amniotic fluid volume
  • Normal amniotic fluid index: 5-25 cm of fluid
  • Oligohydramnios: less than 5 cm
  • Polyhydramnios: greater than 25 cm is considered
28
Q

Maternal Changes During Pregnancy

hormonal changes

A
  • beta-hCG: peaks at wk 9; produced by placenta; maintains activity of corpus luteum until 12 wks
  • estrogen: produced by corpus luteum –> placenta; increases throughout pregnany w/ rapid decline before birth to prepare body for delivery
  • progesterone: produced by corpus luteum –> placenta; increases throughout pregnany w/ rapid decline before birth; maintains uterine lining + smooth muscle relaxant
29
Q

Maternal Changes During Pregnancy

Uterine Changes

A

Increased Uterine Size
1. Hypertrophy of uterine wall leading to more fibrous + elastic tissue
2. Growth is initiated by increased estrogen levels
3. Growth slows by 28 wks but uterus continues to stretch + thin
4. monitor through fundal height measurements

Muscle Contraction
1. uterus is maintained by elevated levels of progesterone
2. Braxton-Hicks Contractions: irregular contractions that do not cause cervical change; more noticeable as pregnancy progresses

Uterine Involution
1. Return of uterus to pre-pregnant state in the several wks post partum

Increased Blood Flow

30
Q

Maternal Changes During Pregnancy

Cervical Changes

A
  1. Cervixsoftens (Goodell’s sign)and can becomebluish (Chadwick sign)due to: increased vascularization + hypertrophy & hyperplasia of cervical glands
  2. Eversion: Glandular cells normally lining the cervical canal become visible on the surface of the cervix; can cause bleeding (should be fully evaluated)
  3. Endocervical mucosal cells produce amucus plug (operculum), an immunological barrier for uterine contents
31
Q

Maternal Changes During Pregnancy

Ovarian/Corpus Luteum Changes

A
  • Ovaries: Follicle-stimulating hormone (FSH) ceases its activity due to the increased levels of estrogen and progesterone secreted by the corpus luteum → placenta
  • Corpus Luteum: enlarges during pregnancy (may form a cyst); supplies progesterone during first 12 wks of pregnancy until placenta takes over
32
Q

Maternal Changes During Pregnancy

Breast Tissue Changes

A
  1. Breast fullness that continues throughout pregnancy
  2. Increased size due to hyperplasia of mammary alveoli and fat deposits
  3. Hyperpigmentation and enlargement of the areola
  4. Enlargement of the Montgomery glands: Sebaceous glands of the areola; Secrete an antibacterial oil that moistens and protects the nipple during breastfeeding
  5. Surface vessels may become prominent due to ↑ circulation: Bluish tint to the breasts

due to increased estrogen + progesterone

33
Q

Maternal Changes During Pregnancy

Colostrum Production

A
  • Occurs by week 16
  • Precursor of breast milk
  • Thin, watery, yellowish secretion with high protein content
  • Thickens as pregnancy progresses
34
Q

Maternal Changes During Pregnancy

Integ System Changes

A
  1. Melasma: “mask of pregnancy”; Brownish hyperpigmentation of the skin over centrofacial-malar area due to ↑ melanocyte-stimulating hormone, estrogen, and progesterone ; Begins at ~16 weeks of pregnancy and gradually increases, Exacerbated by sun exposure; fades after delivery
  2. Hyperpigmentation: Areola of the nipples, Perineum, Linea nigra (Dark line that runs from the umbilicus to the symphysis pubis and may extend as high as the sternum; fades after delivery but might not disappear), Umbilicus
  3. Stretch Marks: Separation within underlying connective tissue of the skin; occurs in areas of maximal stertch (belly, thighs, breasts, butt); fade but never disappear
  4. Sweat Glands: increased activity throughout the body –> profuse persipiration
  5. Misc Changes: spider angiomas, palmar erythema, worsening varicosities; nail changes (brittle or Beau’s lines)
35
Q

Maternal Changes During Pregnancy

Blood Volume Changes

A
  • Increased plasma volume gradually by 30-50% (1500 ml to 3 units): ↑ estrogen → stimulation of the renin-angiotensin system → ↑ levels of circulating aldosterone; aldosterone promotes renal Na+ reabsorption and water retention
  • Results in decrease concentration of red blood cells and hemoglobin: Dilutional anemia; Diagnosis of anemia if the hemoglobin falls below 10.5 g/dL and the hematocrit drops below 30%
  • Hypervolemia of pregnancy compensates for material blood loss at delivery (avg loss vaginal is 400-500cc, for CS is 1000cc)
36
Q

Maternal Changes During Delivery

Heme Additional Changes

A
  • RBC Mass: human placental lactogen (human chorionic somatomammotropin) produced by the placenta; promotes erythropoiesis by enhancing the effects of erythropoietin and increasing RBC production & utilization of iron (note: fetus will steal iron from mother so it is not deficient)
  • Hypercoagulability: 50% increase in blood co ag factors (I, II, VII, VIII, X, XII)
37
Q

Maternal Changes During Pregnancy

CV system- heart displacement + Cardiac Output

A

Heart displacement
1. Heart rotates in response to uterine enlargement and diaphragmatic elevation
2. Left-upward displacement (15-20 degree shift to the left on electrical axis)
3. Apical beat (point of maximum intensity) shifts laterally

Cardiac output
1. CO = SV x HR
2. ↑ CO of 30-50% in the 1st & 2nd trimester to accommodate hypervolemia
3. SV ↑ and reaches maximum at 12-24 weeks gestation (but is position dependent: supine ↓ SV)
4. HR ↑ after 20 weeks…average increase of ~10 beats/min

38
Q

Maternal Changes During Pregnancy

CV System- Venous Return + peripheral vascular resistance

A

Venous Return
1. reduced return because of vena caval obstruction by enlarging gravid uterus
2. Supine Hypotensive Syndrome: 10% of pts in the 3rd trimester; sensitive to caval compression; sx include hypotension, bradycardia, syncope; encourage lateral positioning

Peripheral Vascular Resistance
1. ↓ in the first trimester due to smooth muscle-relaxing effects of progesterone and ↑ production of vasodilators (prostaglandins, nitric oxide, etc.)
2. at time of delivery: ~40% decrease

39
Q

Maternal Changes During Pregnancy

Blood Pressure Changes

A

Arterial pressure
1. ↓ in systolic (4-6 mm Hg) and diastolic (8-15 mm Hg) pressure with a maximum by 20-24 weeks
2. Most often returns to normal by term
3. ↑ BP may be an indicator of preeclampsia

Venous pressure
1. Progressive ↑ in the lower extremities due to compression of the vena cava by the gravid uterus → edema and varicosities
2. ↓ in the lower extremities immediately after delivery

40
Q

Maternal Changes During Pregnancy

Blood flow, strenuous exercise, murmurs, heart sounds, rhythms

A
  • Increased flow: uterus (increasing w/ gestational age), kidneys, skin (hands + feet), breasts
  • Strenuous Exercise: diverts blood flow to large muscles decreasing uretoplacental perfusion; discuss exercise plans with provider
  • Murmurs: low grade systolic ejection murmurs in 90% of pts; diastolic murmurs NOT normal
  • Heart Sounds: second heart sound split with inspiration; S3 gallop after mid pregnancy
  • Rhythm: reduced threshold for re-entry SVT; normal findings include a sinus tachy or brady + isolated premature atrial or ventricular contractions
41
Q

Maternal Changes During Pregnancy

Pulmonary System Changes

A
  • Changes occur due to increased oxygen demand of the mother and fetus
  • Primarily mediated by progesterone
  • Thorax enlargement: Changes due to uterine enlargement; Diaphragm is elevated ~4-5 cm; Rib cage is displaced upward creating a ~2 cm diameter and 6 cm circumference increase in the lower thorax
  • Lung Volume + Capacity: reduced TLC + residual capacity due to elevation of diaphragm; pregnancy induced bronchodilation; slight increase in tidal volume + inspiratory capacity
  • Respiratory Rate: increases to 18-20/min due to increase oxygen consumption; hyperventilation can occur (progesterone increases sensitivity to CO2; can cause resp alkalosis w/ metabolic compensation)
42
Q

Maternal Changes During Delivery

Bladder + kidneys

A

BLADDER
* Displaced upward and is flattened by the enlarging uterus which can cause increased urinary frequency
* ↓ bladder tone as a result of smooth muscle relaxation by progesterone (poor contraction for emptying)
* ↑ bladder capacity and ↑ residual volume…risk for urinary tract infection

KIDNEYS
* Increased functional activity to maintain fluid, solute, and acid–base balance in response to the marked activity of the cardiorespiratory systems
* Enlargement of the kidneys
* Dilation of the urinary collecting system (Predisposing the patient to ascending urinary tract infections)
* Displacement of the enlarging uterus slightly to the right by the sigmoid colon → pressure on the right ureter (Potential for urine stasis, hydronephrosis, and pyelonephritis)

43
Q

Maternal Changes During Pregnancy

Renal Function Changes

A
  • Functional changes are the result of an increase in renal perfusion → ↑ glomerular filtration rate (GFR)
  • ↑ excretion of urinary glucose; Trace of glucose on routine “dipstick” evaluation is normal
  • ↑ excretion of amino acids and water-soluble vitamins (B12 and folate)
  • Slight increase in protein loss althrough proteinuria during pregnancy could indicate underlying pathology (renal disorder); >300 mg per dayis considered high
  • ↑ creatinine clearance → ↓ serum creatinine and ↓ blood urea nitrogen (BUN)
  • All components of the renin–angiotensin–aldosterone system increase during pregnancy
  • ~80% of the glomerular filtrate is reabsorbed by the proximal tubules
  • Aldosterone – sodium reabsorption in the distal tubules
  • Vasopressin – free water regulation → determines urine concentration
  • Decreased specific gravity = dilute urine
44
Q

Maternal Changes During Pregnnacy

GI System

A
  • Displacement of the stomach and intestines due to the enlarging uterus
  • Portal vein enlargement due to increased blood flow
  • Smooth muscle relaxation by progesterone: Lower esophageal sphincter tone, reduced ↓ GI motility, Impaired gallbladder contractility
  • Gastroesophageal reflux: Results from imbalance between the lower intraesophageal pressures and increased intragastric pressures, combined with the lower esophageal sphincter tone
  • Gallstones and cholestasis of bile salts: Reduced gallbladder contractility+ Estrogen-mediated inhibition of intraductal transportation of bile acids
  • Constipation: Mechanical obstruction of the colon due to the increasing size of the uterus + Reduced GI motility + Increased water absorption during pregnancy
45
Q

Maternal Changes During Pregnancy

Metabolism

A
  • Increases in nutritional requirements: ↑ rest to conserve energy and enhance fetal nutrition; Appetite and food intake increases; Food cravings (pica)
  • Weight gain and altered body shape: Average weight gain: 12.5 kg (27.5 lbs); Uterus and contents, breast tissue, blood volume, water volume (extravascular and extracellular) fluid, deposition of fat and protein
  • Weight loss (early pregnancy): Nausea and vomiting or “morning sickness”; 4-8 weeks gestation → resolves by 14-16 weeks; Severe form is known as hyperemesis gravidarum…weight loss, electrolyte imbalance, and ketosis
  • Lack of proper nutrition may be an indication of intrauterine growth retardation (IUGR) of the infant
46
Q

Ovaries

anatomy

A
  • Adnexal structure
  • Produce numerous follicles every month, with one dominant follicle maturing → ovulation
  • Suspended laterally to the uterus by the utero-ovarian ligament
  • Covered by the mesovarium (component of the broad ligament)
  • Connected to the pelvic wall by the suspensory ligament
  • Blood supply: ovarian artery, a direct branch of the aorta, and the uterine artery
47
Q

Breast Cancer

DCIS vs LCIS

non-invasive

A

Ductal carcinomain situ(DCIS)
1. Proliferation of cytologically malignant cells within the mammary ductal system, with no invasion of the surrounding stroma
2. ⅓ develop invasive cancer in 5 years
3. Frequently detected bymammography

Lobular carcinomain situ(LCIS)
1. Proliferation of malignant cells within thelobules, growing in an incohesive manner
2. Rarely with calcifications
3. Low risk for invasive breast cancer

48
Q

Breast Cancer

IDC vs ILC

invasive breast cancer

A

Infiltrating ductal carcinoma (IDC)
1. Most common invasive breast cancer(76% of all breast carcinomas)
2. Mostly unilateral
3. Gross appearance: Firm,fibrous, “rock-hard”masswith irregular stellate shape; Often 2–3 cm in size
4. Metastasizes early

Infiltrating lobular carcinoma (ILC)
1. 2nd most common invasive breast cancer (5%–10%)
2. Usually multicentric and present bilaterally
3. Gross appearance:May not have amasslesion; Difficult to palpate or detect bymammography
4. Metastasizes late

49
Q

Breast Cancer

Paget’s Disease of the Breast

A
  • 1%–4% of cases
  • Gross appearance:
  • Unilateral eczematous, erythematous patcheson thenipple, andnipple retraction
  • With palpablemass (> 50% of cases) → invasive carcinoma, ER negative andHER2 overexpression
  • Without amass → DCIS
50
Q

Breast Cancer

describe use of mammograms for screening + types of mammograms

A
  • Most effective method of detecting earlybreast cancer
  • Screeningmammogram: performed on a woman with no symptoms or signs ofbreast cancer
  • Diagnosticmammogram: performed on a woman who has a breast lesion suspicious for cancer either on clinical grounds or by findings on a screening mammogram

Types:
1. Screen film mammography: mostly replaced by digital mammography in the United States
2. Digital mammography: preferred for densebreasts(approximately 50% of all women)
3. Digital breast tomosynthesis (BDT, “3-D mammography”): Takes images from many angles to obtain a 3-dimensional picture, improves thesensitivity and specificityof mammography, preferred modality by the American College of Breast Surgeons
4. Computer-aided detection (CAD): Artificial intelligence (AI) technique that uses pattern recognition to highlight suspicious features and marks the features for the radiologist to review

51
Q

Breast Cancer

BI-RADS screening Strategy

A
  1. BI-RADS 0: recommend additional imaging (mammogram or targeted US)
  2. BI-RADS 1: negative; continue routine MR screening
  3. BI-RADS 2: benign; continue routine MR screening
  4. BI-RADS 3: probably benign; 6 mo follow up screen
  5. BI-RADS 4: suspicious; tissue bx
  6. BI-RADS 5: highly suggestive for malignancy; issue bx
  7. BI-RADS 6: bx proven malignancy; excise
52
Q

Vulvar Lesions

anatomy review of bartholin glands

A
  • Also called thegreater vestibular glands
  • Paired glands located on both sides of thevestibule(space between thelabia minora, which opens into thevagina)
  • Secrete lubricating mucus into thevestibuleduring sexual arousal
    • Ducts: Approximately 2.5 cm in length, Open into thevestibuleat ~5 and ~7 o’clock positions
53
Q

Amenorrhea

HPO axis general players

A
  • Hypothalamus: the pulse generator; releases GnRH (gonadotropin releasing hormone) which is down regulated by Dopamine, endogenous opioids
  • Pituitary: releases FSH (follicle stimulating hormone), LH (luteinizing hormone) when stimulated by GnRH; down regulated by TSH, Prolactin
  • Ovary: releases Estradiol (E2) and Progesterone; some Testosterone
54
Q

Amenorrhea

HPO asxis full cycle

A
  • GnRH - based on pulse frequency releases two types of hormones FSH/LH
  • Hypothalamus releases GnRH which tells the pituitary to release FSH
  • FSH tells the ovary to release estradiol, increase oocyte formation, allows testosterone to metabolize into estradiol and creates inhibin release
  • FSH and inhibin biofeedback to hypothalamus to stop GnRH/FSH production
  • E2 levels rise causing feedback to hypothalamus to change GnRH frequency
  • GnRH tells pituitary to release LH which then tells the ovary to ovulate, form oocyte remnant into corpus luteal cyst which then produces progesterone
  • HCG binds to LH receptor allows corpus luteum to be maintained
55
Q

Amenorrhea

PE findings with anatomic imperforate hymen

A

Bulging blue membrane at hymen (hematocolpos)

This distention of the vagina may cause back pain, pain with defecation, or difficulties with urination

56
Q

AUB

FSH Overview

A
  • Tells the ovary to start to grow “the follicle of the month”
  • FSH – high during pre-puberty and menopause – roughly 30-100
  • FSH – low during prime fertility – teens through 30’s - < 10
  • FSH – subfertility levels 10-15 in the 30-40’s.
57
Q

AUB

estradiol + progesterone

A
  • Estradiol is elevated during fertility and starts to fall during perimenopause hot flashes
  • Estrogen helps grow the endometrial lining to make a “happy home”
  • A peak in estrogen signals LH to surge which leads to ovulation
  • Progesterone helps support and stabilize the uterine lining
  • Progesterone levels fall after pregnancy is not achieved and this triggers the uterine lining to shed
  • Also progesterone is the “sappy” hormone – when falling causes mood swings – hello PMS.
58
Q

AUB

follicle/cyst formation

A
  • Follicles are mature at 20-30mm
  • Corpus luteal cysts can get to 40mm
  • Ovulation pain – mittelschmerz
59
Q

AUB

normal menstural flow

A
  • Frequency 21-35 days
  • Duration is normal 10 days or less, although average is 5 days
  • Now average age of menarche is 12 y/o and menopause is 51 y/o
  • According to AAP – precocious puberty is under 8 y/o for girls
60
Q

AUB

PALM COEIN for etiologies of AUB

A

PALM – structural issues
* P: Polyp
* A: Adenomyosis
* L: Leiomyoma (further explained by submucosal – AUB-Lsm)
* M: Malignancy and hyperplasia

COEIN: nonstructural causes
* C: Coagulopathy
* O: Ovulatory
* E: Endometrial
* I: Iatrogenic
* N: Not yet classified

61
Q

Cervical Cancer

Why to do HPV testing

A
  • better at detecting CIN 2+
  • Cytology is about 50-80% sensitivity
  • HPV testing >90% sensitivity
  • Also cytology is not effective in adenocarcinoma or AIS detection
  • Cytology was read negative in over half of women 25-29 y/o with CIN3+
  • Although prevalence of HRHPV is 21.9% in 25-29y/o: HPV 16 is only 5.3% and HPV 18 is 1.6%
62
Q

Cervical Cancer

when to stop screening

A
  • 65 yrs with adequate negative prior screeing and no CIN2+ in last 25 yrs
  • Adequate neg screening = 3 consecutively neg paps or 2 consecutive neg HPV tess
  • if hysterectomy w/ removal of cervix w/ no hx CIN2+
  • NOTE: if surgical history of “freezing the cervix” or “burned some cells”, continue because we DO NOT know pathology
63
Q

Cervical Management

A

CMT (78 decks)

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