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Med School > Abnormal Uterine Bleeding > Flashcards

Abnormal Uterine Bleeding Flashcards

1
Q

Primary vs. Secondary Amenorrhea

A

Primary - no menses by 14 and no secondary sexual characteristics OR no menses by 16 with secondary sexual characteristics

Secondary - previous history of menstruation with no menses for 3 cycles (or 6 months)

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2
Q

Outline the control pathway from the CNS to the uterus

A

CNS –> Hypothalamus (GnRH) –> Anterior Pituitary (FSH/LH) –> Ovaries (estrogen/progesterone) –> uterus –> menses

*estrogen and progesterone feedback on the hypothalamus and pituitary

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3
Q

Important ROS Questions to rule out a hypothalamic cause?

A
  • radiation, trauma, diet, stress, chronic illness, eating disorders, headache, vision changes, anosmia (Kallman’s)
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4
Q

Important things to examine on physical?

A
  • growth record, neuro, thyroid, tanner staging, abdo exam, genitals (estrogen status, imperforate hymen), acne, hirsutism
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5
Q

Important labs/ tests?

A
  • day 3 FSH/LH/PRL/TSH/E2
  • day 21 progesterone/ BHCG
  • CBC, ferritin, VW factor, coags, renal/liver, pap/swabs
  • karyotype
  • progesterone challenge (helps determine estrogen status)
  • androgens (DHEA, testosterone, 17-OH progesterone) if symptoms
  • pelvic U/S, MRI head if progesterone challenge (-)
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6
Q

Hyper vs Hypogonadotropic Hypogonadism

A

Hyper –> ovaries are failing (FSH/LH high, estradiol low)
–> do a karyotype (can have chromosome issue)
Hypo –> CNS failing (FSH/LH low, estradiol low)

*43% of primary amenorrhea is HYPER, 31% is HYPO, 26% is EU (chronic anovulation/ outflow tract issue)

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7
Q

Examples of HYPOgonadotropic Hypogonadism

A
  • structural or endocrinologic CNS issue (test with MRI head) OR stress/anorexia/excessive exercise/hypothyroidism/etc.
  • adenoma, prolactinoma, craniopharyngioma, FSHB mutation, idiopathic
  • Kallman’s –> isolated GnRH deficiency, anosmia, mid face defects
  • Sheehan’s –> pituitary stops working after significant blood loss during childbirth
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8
Q

Examples of EUgonadotropic Eugonadism (causes of bleeding)
- common tests
- elaborate on each and tx

A
  • PCOS –> 2 of Androgen excess, ovulatory dysfunction, polycystic ovaries
  • tx with regular progestin withdrawal (prevents endometrial hyperplasia)
  • Hyperprolactinemia –> high PRL and low/normal FSH/LH
  • can be caused by meds, prolactinoma, hypothyroidism
  • treat with dopamine agonist (bromocriptine, cabergoline)
  • Outflow Tract Abnormalities –> congenital (imperforate hyymen, vaginal septum, cervical or mullerian agenesis) or acquired (Ashermann’s intrauterine adhesions)
  • test with physical exam, TSH/PRL/androgens/ progesterone challenge, U/S
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9
Q

How does a progesterone challenge test work?

A
  • gives an estimate of the concentration of estrogen (confirms estrogen primed uterus)
  • medroxyprogesterone 5-10mg or micronized progesterone 200-300mg daily for 5-10 days
  • A positive response is normal withdrawal bleeding for 3-5 days about 2-10 days after the end of the progestin
  • A positive repsonse suggests E2 is >50pg/mL
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10
Q

What is Mullerian Agenesis (MRKH)?
- Tx?

A
  • defect in the AMH gene
  • will have normal breasts, ovaries, pubic hair
  • NO uterus, cervix, upper vagina
  • renal and skeletal abnormalities are also common

Tx - vaginal dilators (#1), psych support, fertility counselling, surgical neovagina

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11
Q

Primary Ovarian Insufficiency (POI) - the only example of HYPERgonadotropic Hypogonadism
- two diff types and their different causes

A
  • causes menopause before age 40

Normal Karyotype
–> chemo/radiation, ovarian surgery, gonadal dysgenesis, infectious oophoritis (mumps) fragile X, Addison’s, thyroid, SLE, T1DM, myasthenia gravis (lots of autoimmune causes)
*Fragile X –> CGG repeats in the FMR1 gene, most common inherited cause of low IQ and autism

Abnormal Karyotype

  1. Turner’s –> 45XO or mosaic variations, short, webbed neck, low ears/hairline, wide nipples/ shield chest, absent sexual development in some
    - treat with hormones/pubertal induction/ gonadectomy/ fertility
  2. Androgen Insensitivity Syndrome –> 46XY, X-linked recessive, mutation in gene for androgen receptor
    - inguinal testes (no sperm), breasts, no pubic hair/uterus, blind vagina
    - treat with gonadectomy if complete, virilization
  3. Androgen Synthesis Disorder –> 5alpha-reductase deficiency (testosterone cannot be converted to DHT), autosomal recessive
    - male internally, female externally
    - treat by virilizing at puberty
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12
Q

General treatments for:
- HYPOgonadotropic hypogonadism
- HYPERgonadotropic hypogonadism
- EUgonadotropic eupogonadism

A

HYPO –> get back to weight you had regular cycle with, decrease stress, ovulation induction with gonadotropins (clomiphene citrate, metformin, drilling if pregnant)

HYPER –> psych, hormones until menopause (combo OCPs), pubertal induction, contraception discussions

EU –> thyroid replacement, dopamine agonist for hyperprolactinemia, healthy weight, regular progestin withdrawal for PCOS, ovulation induction if pregnant

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13
Q
  • If uterus absent, what tests should you order?
  • If withdrawal bleeding on progetserone bleeding is present and normal LH/FSH?
  • both deficient estrogen or progesterone can lead to…
    *Bright red bleed is likely…
A
  • karyotype, serum T/E2, LH/FSH
  • chronic anovulation
  • bleeding
  • acute
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14
Q

Abnormal Uterine Bleeding Defintion

A
  • change in the frequency/ duration/ amount of menses
  • chronic if over 6 months
  • peak prevalence prior to menopause
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15
Q

Most common causes of hysterectomies?

A
  • menorrhagia, fibroids
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16
Q

Overview of the menstrual cycle

A
  • LH peak during ovulation (and smaller FSH peak)
  • must have estrogen exposure first, then both E+P, then withdrawal of both
  • in the early follicular phase the endometrium is thin, in the luteal phase it is thick
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17
Q

Factors that stop bleeds vs. promote bleeds?

A

Stop
–> progesterone dependent (early)
–> normal coagulation cascade (late)
–> Endothelin-1 and PG-F2a (vasoconstriction)

Promote
–> excess PGE2 and PG12 (vasodilate)
–> excess plasminogen activators (breakdown clot)
–> deficiencies in endometrial repair

*see higher levels of PGE2 and PG12 in women with menorrhagia

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18
Q

Typical length of cycles over time?

A
  • first 5-7 years are commonly longer (though some will have short) due to immature HPO axis
  • slowly become shorter with more cycle per year
  • 8-10 years before menopause they lengthen again (less quality and quantity of eggs)
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19
Q

Menopause

A
  • Permanent loss of menses due to loss of follicular activity
  • 12 months of amenorrhea (since LMP) with no obvious pathological cause (still need contraception if ur still bleeding!)
  • 99% of menopause is after 40, average age is 51.5
  • low estrogen and high FSH
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20
Q

Length of a menstrual cycle and amount of blood lost

A
  • typically every 28 days (+/- 7)
  • lasts 4 days (+/- 2)
  • 40cca (+/- 20)

*after ovulation is fixed (13-15d), but beforehand is variable

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21
Q

Definition of an Irregular Cycle

A
  • in first 1-3 years –> under 21 days or over 45 days
  • between 3 years and menopause –> under 21 days or over 35 days
  • ANY cycle over 90 days or less than 8 a year

*a signal of oligo/anovulation

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22
Q

Definition of:
- Menorrhagia
- Metrorrhagia
- Menometrorrhagia

A
  • over 7 days or over 80cc bleeding at regular intervals
  • bleeds at irregular but frequent intervals, variable amounts
  • prolonged uterine bleeds at irregular intervals
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23
Q

PALM-COIEN

A

Structural –> Polyps, Adenomyosis, Leiomyoma, Malignancy/ hyperplasia

Non-Structural –> Coagulopathy, Ovulatory dysfxn, Iatrogenic, Endometrial, Not yet classified

*always want to exclude pregnancy or cancer!

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24
Q

Drugs that may cause AUB?

A
  • SSRIs/TCAs, anticonvulsants, anticoagulants, contraception, steroids, antispychotics, tamoxifen
  • chasteberry, ginseng, danshen
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25
Q

When is anovulatory bleeding considered normal (physiological)?

A
  • Adolescence, perimenopause, lactation, pregnancy
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26
Q

Common unique causes of bleeding for:
- at birth
- 48-52
- 52+

A
  • at birth - estrogen withdrawal
  • 48-52 - an-ovulation due to perimenopause, endometrial hyperplasia, cervical and endometrial cancer
  • 52+ - hormone therapy, vaginal/endometrial atrophy, endometrial cancer
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27
Q

Perimenopause

A
  • typically ~5 years
  • early on has variable cycle length, but overall lenghtneing (40-50 days)
  • late has 2 or more skipped cycles (anovulation), erratic menstruation
  • FSH and LH increase (though also fluctuating), estrogen fluctuates widely but is long term decreasing
    *cannot predict menopause based on FSH
  • may be most symptomatic during this time!
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28
Q

Signs of Hypothalamic Amenorrhea

A
  • GnRH pulsatility is low, LH/FSH low, estrogen very low
  • thin endometrium, vaginal atrophy, low bone density
29
Q

PCOS

A
  • hyper-estrogenic endometrium with failure of regular exposure to progesterone (THICK)
  • normal FSH and estrogen, LH can be increased, increased androgens
  • risk of endometrial hyperplasia and cancer
30
Q

Investigations for structural problems? Indications for endometrial biopsy?

A
  • Pelvic/ transvaginal U/S, saline infusion sonogram, hysteroscopy, biopsy
  • tend to have normal ovulatory cycles
  • 40+, failure of tx, hx of anovulatory cycles, significant bleeding outside of menses, post-menopause, endometrial thickness over 4mm on TVUS (although honestly do it even if its smaller)
  • over 90kg, nulliparous, PCOS, DM (risks for endometrial cancer)
31
Q

Endometritis/ Cervicitis
- signs
- common causes

A
  • purulent discharge, post-coital bleeding, pelvic tenderness, fever
  • commonly chlamydia and gonorrhea
32
Q

HPV
- high risk strains
- low risk strains
- virility factors

A
  • can cause oropharyngeal (80% men), anal, penile, vulvar, cervical cancers and lead to genital warts, can be asymptomatic
  • most common STI (50% of people get it)

High risk - 16/18/31/33/45/52/58 (cancers)
Low risk - 6/11 (genital warts, respiratory papillomatosis, oral/conjunctival papillomas)
* 16 and 18 are most common

  • E6/E7 oncoprotein mediate cervical cancer –> interfere with tumor supressor proteins, insert into DNA, lead to dysplasia, once it invades (cancer)
33
Q

LSIL vs HSIL (cytology findings)

A
  • low grade intraepithelial lesion –> CIN I, mild cervical dysplasia, HPV infection and virus production
  • high grade intraepithelial lesion –> CIN II (moderate cervical dysplasia, no virus production), CIN III (severe cervical dysplasia/ carcinoma in situ/ invasive carcinoma - increased E6/7 and viral DNA integration)

*LSIL/HSIL are cytology (pap) terms, CIN is a histology term

34
Q

Risks for HPV/ Cervical Cancer

A
  • early age first sexual activity (lower immune response), mutliple partners, multiparity, long term OC use, immune compromise (smoking, steroids, DM, HIV, renal failure)
35
Q

HPV Vaccine
- different forms
- schedule

A
  • best prevention for cervical cancer
  • greatest benefit if before onset of sexual activity
  • non-infectious recombinant vaccine

HPV2 (Cervarix) - 16/18, 10-25 females
HPV4 (Gardisil) - 6/11/16/18, 9-26 males and females
HPV9 (Gardisil-9) - 6/11/16/18/31/33/45/52/58 (prevents 90% of cancers)

9-14 –> 2 doses at 0/6m
15+ –> 3 doses at 0/2/6m
also 3 doses if HIV, stem cell/ organ transplant, immune deficits
*currently gender neutral vaccination in grade 6 in BC, available to women/queer men/HIV/transgender 9-26 for free

36
Q

Secondary Prevention of HPV

A
  • visual inspection with acetic acid (VIA)
  • cytology (pap smear, very specific but low Sn)
  • HPV testing (High Sn, slightly lower SP, actually more effective) done every 5 years
37
Q

Treatment for Surgical Dysplasia

A
  • LEEP (loop electrosurgical excisional procedure) for stage IIB (cancer outside cervix)
38
Q

When to screen for cervical cancer?

A
  • Anyone with a cervix starting at 25 or 3 years after 1st sexual activity (even if same sex, transgender, received the vaccine)
  • Not necessary if no sexual contact or TOTAL hysterectomy
  • Discontinue at 69 (as long as 3 negative paps in the last 10 years)
  • Done yearly until 3 negative results in a row, then every 3 years
39
Q

If uterus is bigger than expected for GA?

A
  • twins, pelvic mass, molar pregnancy, wrong dates
40
Q

Gestational Trophoblastic Disease (GTD)

A
  • group of diseases that occur during pregnancy as a result of abnormally proliferating trophoblast cells
  • pre-malignant –> hydatidiform mole or molar pregnancy (partial/ complete)
  • malignant –> gestational trophoblastic neoplasia (GTN)

*high risk picture –> uterine bleeding, profuse vomiting, 42 yo at 10w gestation

41
Q

Normal journey from zygote onwards (this is all occuring before implantation)
- what forms the embryo vs palcenta?
- what produces BHCG?

A
  • Zygote –> 12-16 cells Morula –> fluid filled cavity Blastocyst
  • Inner Cells –> embryoblasts (become embryo)
  • Outer cells –> trophoblasts (become placenta)
  • trophoblasts differentiate into cyto and syncitiotrophoblasts which invade the endometrium to the maternal spiral arteries (very agressively invasive)
  • syncitio produce BHCG which maintains the corpus luteum and progesterone until placenta is fully formed, also responsible for morning sickness
42
Q

Hydatidiform Moles
- what are they?
- two different types

A
  • abnormal fertilization resulting in atypical trophoblast cell proliferation, tumours that arise from gestational tissue
  • Complete Mole –> ovum fertilized by haploid sperm which then duplicates OR fertilized by 2 sperm (ovum nucleus deactivated or absent)
  • 46XX or rarely 46XY, paternal origin
  • absent fetus, large uterus, BHCG over 100,000
  • widespread villous edema, marked trophoblast atypia, snowstorm pattern on U/S
    -15-20% GTN risk
  • Partial Mole –> ovum fertilized by 2 haploid sperm (haploid ovum nucleus still activated)
  • 69XXX or rarely 69XXY, maternal (1) and paternal (2) origin
  • present fetus, small uterus, BHCG under 100,000
  • focal villous edema, mild trophoblast atypia, multicystic placenta on U/S
  • 1-5% GTN risk
43
Q

Common clincial presentation of a complete mole
- test to order and why?

A
  • missed/late periods, vaginal bleeding in the first trimester, hyperemesis, abdominal pain, HYPERth sx, large uterus, absent fetal HR, ovarian enlargement on U/S, snowstorm pattern on U/S
  • order TSH as it bears structural resemblance to BHCG, and BHCG can bind to the TSH receptor and cause elevated T4 and low TSH
44
Q

Risks for molar pregnancy

What is considered high risk?

A
  • previous molar pregnancy
  • extremes of reproductive age (under 20 over 36), asian and hispanic heritage
45
Q

Management of Molar Pregnancy

A
  • prepare for complications with TH/T4/BHCG/CXR, etc.
  • suction and curettage under general anesthesia, send tissue for pathology
  • Post-evacuation contraception and BHCG @48h, weekly until undetectable, monthly for 6m (serial BHCG helps monitor for persistent malignant disease as it is a tumor marker for GTD, also want to take contraception to ensure an increase in BHCG isn’t because of a new pregnancy)
    –> OCP or injectable medroxyprogesterine acetate is preferred, IUDs not recommended (perforation)
  • in subsequent pregnancies, need U/S @6-8 weeks and BHCG measured 6 weeks post-partum
46
Q

Gestational Trophoblastic Neoplasia (GTN)
- 3 diff types
- prognosis
- how to dx
- treatment

A
  • more common after a molar pregnancy but can happen at any time
  • invasive mole (more common in complete)
  • choriocarcinoma
  • placental site trophoblastic tumor (rare)
  • over 95% 5 year survival, fertility is unaffected, normal offspring, 98% will have normal pregnancy after
  • high risk if metastases (lungs most common), BHCG over 40,000, over 4 months since pregnancy, failed chemo
  • over 10% increase in BHCG for 3+ values over 2 weeks OR
  • plateau of BHCG for 4 measurements over 3 weeks
    OR
  • BHCG remains high for 6 months
    OR
  • histological carcinoma of choriocarcinoma

*other investigations include CXR (CT/MRI of abdo/pelvis/head) if abnormal, NEVER biopsy

Tx
–> low risk –> single chemo agent (methotrexate or actinomycin D)
–> high risk –> combo chemo (MTX, actinomycin D, and cyclophosphamide)
*radiotherapy if cerebral metastases

47
Q

Ovarian Reserve
- how to test

A
  • ovaries contain all eggs at birth (1-2 million, actually more as a fetus @20 weeks), menopause has under 1000
  • test with day 3 FSH, over 20 is menopausal
  • antral follicle count
  • Anti-mullerian hormone (AMH) - made by the granulosa cells of pre/small antral follicles, 0.1pmol/L (low) is menopausal
48
Q

What causes accelerated loss of primordial follicles?

A
  • smoking
  • chemo, pelvic radiation
  • ovarian surgery
  • potentially autoimmunity

*Primordial follicle –> prenatal follicle –> antral follicle –> preovulatory follicle

49
Q

What produces LH/FSH and what do they control?

A

LH - stimulate theca cells in ovarian stroma (androgens)
FSH - stimulate granulosa cells in ovarian follicle (estrogens)

*both from anterior pituitary

50
Q

Explain the mechanism that results in low estrogen high FSH in menopause

A
  • no oocytes –> no follicles –> no granulosa cells –> no estrogen and no inhibin B
  • inhibin B normally lowers FSH level (also a marker of follicle #)
51
Q

Symptoms of Menopause

A
  • vasomotor –> hot flashes, night sweats, issues sleeping
  • psych –> worse PMS, depression, irritable, poor memory and concentration (best predictor is prior depression)
  • sexual dysfxn –> dyspareunia, dryness, low libido
  • somatic –> headache, dizziness, arthralgias, palpitations, dry itchy skin
  • stress incontinence > urge incontinence
  • weight gain (~5lbs) due to lower metabolism and shift in fat composition
52
Q

Hot Flashes
- physiology
- tx

A
  • heat starting in chest and rising, last 3-4 minutes, +/- anxiety and palpitations
  • # 1 reason for hormone therapy, 80% of women
  • likely hypothalamic, thermoregulatory dysfunction due to low estrogen
  • narrowing of the thermoneutral zone, kisspeptin (hypertrophy, interact more with thermoregulatory centers), neurokinin B, dynorphin neurons
  • some placebo effect
  • evidence - weight loss, CBT, clinical hypnosis
  • meh - mindfulness, paced respiration, soy and ferment extract
  • can also try SNRIs/SSRIs/gabapentin/clonidine/oxybutynin
53
Q

Hormone Therapy
- goals
- schedule
- if under 45?
- examples (estrogen, progesterone, other)

A
  • aim is to lower estrogen deficiency symptoms, treat urogenital atrophy, and prevent osteoporosis
  • for estrogen no specific time frame or dose, can continue past 65+, do NOT give if asx
  • Cyclic –> daily estrogen and progesterone 12-14 days a month, will induce withdrawal bleeding
  • Continuous –> daily estrogen and daily progesterone, no bleeding
  • if under 45, hormone REPLACEMENT therapy until average age of menopause (premature menopause has risk of osteoporosis, CV disease, low cognition, early mortality)

Estrogen
- most potent is ethinyl estradiol (synthetic 17B-estradiol), though actually not included in guidelines. Can be given PO, transdermal patch, transdermal gel, injection
- also premarin (conjugated estrogen)

Progesterone
- want enough to prevent endometrial hyperplasia
- oral medroxyprogesterone, oral micronized progesterone, Norethindrone acetate, Levonorgestrel IUD (Mirena/Kyleena - Mirena is higher dose)

Other
- Tibolone - estrogenic, progestogenic, and androgenic properties
- Tissue Specific Estrogen Complex - selective estrogen receptor modulator which prevents endometrial hyperplasia
*do not need endometrial protection with progesterone with these

54
Q

When should you consider transdermal hormone therapy?

A
  • smoker, shift worker, high TGs, HTN, gallbladder disease, sexual dysfucntion, migraines, malabsorption, high VTE risk, metabolic syndrome
55
Q

Endometrial Cancer
- risks
- sx
- dx
- tx - if premenopausal?

A
  • most common gyne cancer in Canada
  • average age is 63, only 15-20% are premenopausal
  • NO SCREENING
  • risks –> unopposed estrogen (thickens lining), menopause after 55, nulliparity, chronic anovulation, HTN, DM, obesity, tamoxifen, HNPCC syndrome
  • sx –> 90% have AVB, asymptomatic post-menopausal bleeding with endometrial cells on pap, perimenopausal AUB with abnormal endometrial cells
  • dx –> endometrial biopsy (can be done in office)
  • also useful: history and physcial, speculum exam, dilation and curettage, hysteroscopy
  • pelvic U/S can only reduce suspicion (endometrium should be under 5mm)
  • tx
    –> low risk –> hysterectomy and BSO
    –> high risk –> hysterectomy, BSO, assessment of LNs, +/- omentectomy
  • radiotherapy THEN chemotherapy with increasing stage and risk factors
  • if premenopausal or grade 1A, can give fertility preserving options –> high dose progestins (Mirena IUD/ Megace), may cause weight gain/ HTN/ VTE
56
Q

Staging of Endometrial Cancer (FIGO)

A
  • Surgical
  • 1A - only endometrium
  • 1B - spread to myometrium
  • 2 - spread to cervix
  • 3A - spread to ovary
  • 3B - vagina
  • 3C - spread to lymph nodes
  • 4A - bladder/bowel
  • 4B - other organs
  • EC extends through the uterus, spreads to the tubes/ovaries/LNs, and eventually the blood
57
Q

What does follow-up for endometrial cancer look like?

A
  • pelvic exam every 3-4 months for 2 years, then every 6 months for 3/5 years
  • most patients with recurrence will be bleeding
  • Paps/ blood/imaging are NOT helpful
  • encourage patients to lose weight, manage HTN/DM, lower CV risks (leading cause of death after EC treatment)
58
Q

Screening for breast cancer? Colorectal cancer?

A
  • mammogram every 2 years from 50-79
  • FIT test every 2 years from 50-74
59
Q

Lynch Syndrome
- screening
- when to test
- tx

A
  • inherited DNA mismatch repair mutation
  • increased risk of endometrial, colorectal, and ovarian cancer
  • test if 3 family members, 2 generations, 1 under 50
  • test even if already diagnosed with EC!
  • screening - colonscopy every 2 years 25-40, annual after 40, annual TVUS and endometrial biopsy 35+, immunohistochemistry for mismatch repair (absence of 4 MMR proteins in tumor), tumor infilitrating lymphocytes and dedifferentiated carcinoma on histology
  • ASA for CRC and OCP and ASA for EC/OC
  • tx –> colectomy, hysterectomy, BSO
60
Q

Most common cause of post-menopausal bleeding?

A
  • benign endometrial carcinoma
61
Q

Fibroids
- sx
- dx

A
  • very common and often asymptomatic
  • common sx are menorrhagia, pelvic pain, infertility, pregnancy loss
  • often first indication is on bimanual exam, but best diagnostic test is TVUS
62
Q

Benign vs. Malignant Postmenopausal Bleed

A

Benign –> atrophic vaginitis, cervical/uterine polyp, fibroids

Malignant –> endometrial cancer/hyperplasia, cervical cancer, vaginal/vulvar cancer

63
Q

What to do if abnormal pap smear?

A

Send for colposcopy

64
Q

Staging Cervical Cancer

A
  • need a biopsy with stroma to determine premalignancy vs. cancer
  • can be done with LEEP or MRI/PET scan

0 - carcinoma in situ (100% survival)
I - confined to cervix
II - beyond cervix but not to pelvic wall or lower 2/3 of vagina
III - pelvic wall or lower 1/3 of vagina
IV - bladder, rectum, metastasis (7% survival)

65
Q

Symptoms, Diagnosis, and Treatment for Cervical Cancer

A

Sx –> bleeding (especially post-coital), discharge

Dx –> Colposcopy and biopsy

Stage I –> radical hysterectomy (ovaries included), bilateral pelvic lymphadenopathy and sentinel pelvic nodes

Stage II-IV –> ONLY radio and chemotherapy

66
Q

AUB investigations in perimenopause

A
  • BHCG, CBC, ferritin, TSH, prolactin, U/S, endometrial biopsy, pap
  • FSH/LH/est/progest are useless as widely fluctuating
67
Q

Contraception in older age
- Absolute contraindications for estrogen contraception

A
  • Age alone is not a contraindication for contraception, but CV risks increase so often switch to progesterone only
  • smoker over 35, personal VTE Hx, migraine with aura, under 6 weeks postpartum, BP >160/100, ischemic heart disease, prior stroke, breast cancer, severe cirrhosis/DM
68
Q

Vasomotor Sx Tx

A
  • HT w estrogen is the most effective treatment for vasomotor symptoms (not at high enough dose to help with contraception or AUB)
  • cold showers, dress warm, avoid coffee/alcohol/ smoking, CBT, sleep, healthy diet/ exercise, hypnosis, etc.
  • low dose combined pill/patch/ring, venlafaxine, clonidine

Med School (21 decks)

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