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womens health Flashcards

1
Q

What are the consequences of menstrual cycle disorders?

A

Negative impact on QOL, reproductive health, long term detrimental health effects (increased risk of osteoporosis with amenorrhea, risk of diabetes with PCOS)

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2
Q

what are the Menstrual Cycle Disorders?

A
  1. Amenorrhea
  2. menorrhagia
  3. dysmenorrhea
  4. premenstrual syndrome
  5. polycystic ovary syndrome
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3
Q

what is Amenorrhea?

A

No menstrual bleeding in a 90 day period

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4
Q

what are the types of amernorrhea?

A
  • Types
    • Primary/ functional
      • Absence of menses by age 15 in females who never menstruated
      • Rare
    • Secondary
      • Absence of menses for 3 cycles in a previously menstruating female
      • Rare, but more common than primary
      • More frequent in <25 yo with history of menstrual irregularities, competitive athletics or massive weight loss
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5
Q

what is the etiology of amenorrhea?

A
  • Anatomical causes: Pregnancy, uterine structural abnormalities
  • Endocrine disturbances leading to chronic anovulation (egg does not release or ovulate)
  • Ovarian insufficiency/ failure
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6
Q

what is the treatment for amenorrhea?

A
  • Identify underlying cause
  • Non-pharmacological: Gain weight/ reduction of exercise intensity/ Stress management
  • Pharmacological: Combined oral contraceptive (COC), Estrogen, Progestin, Copper IUD
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7
Q

what is Menorrhagia?

A
  • Heavy menstrual bleeding
  • Menstrual blood loss >80ml per cycle OR Bleeding >7d per cycle
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8
Q

what is the pathophysiology of Menorrhagia?

A

Uterine-related factors
- Fibroids (benign tumors growing in or on uterine wall)
- Adenomyosis (endometrial tissue grows into muscular wall of uterus)
- Endometrial polyps
- Gynecologic cancers
- Alterations in hypothalamic-pituitary-ovarian (HPO) axis

Coagulopathy factors
- Cirrhosis
- von Williebrand disease (deficiency of pro-von Willebrand factor)
- Idiopathic thrombocytopenic purpura (abnormal decrease in platelets)

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9
Q

how to treat Menorrhagia?

A
  • Contraception: COC/ Progestin IUD/ Progestin only oral contraceptive/ Progestin injection
  • Non-contraceptive: NSAIDs during menses/ Tranexamic acid (clots blood) during menses/ Cyclic progesterone
  • Endometrial ablation: Destroy endometrial lining of uterus
  • Hysterectomy: Remove entire uterus
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10
Q

what is Dysmenorrhea?

A
  • Crampy pelvic pain with or just before menses
  • Primary and secondary
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11
Q

how does Dysmenorrhea happen?

A
  • For primary: Release of prostaglandins and leukotrienes —> Vasoconstriction —> Cramps
  • For secondary: Endometriosis (tissue similar to lining of uterus (endometrium) grows outside uterus)
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12
Q

how to treat Dysmenorrhea?

A
  • Nonpharacological: Topical heat therapy, exercise, acupuncture, low-fat veg diet
  • Pharmacological:
    • First line: NSAIDS
    • Second line: COC
    • Third line: Progestin injections/ IUD (BUT can cause render amenorrhea 😖)
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13
Q

what is Premenstrual syndrome (PMS)?

A
  • Cyclic pattern of symptoms occurring 5 days before menses that resolve at onset of menses
  • Does not impair daily activities
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14
Q

what are the symptoms for Premenstrual syndrome (PMS)?

A
  • Somatic (physical): Bloating, headache, weight gain, fatigue, dizziness/ nausea, appetite changes
  • Affective (mood): Anxiety/ depression, angry outburst, social withdrawal, forgetfulness, tearful, restlessness
    • Severe: Premenstrual dysophoric disorder (PMDD) —> Psychiatric condition
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15
Q

how to treat Premenstrual syndrome (PMS)?

A
  • Selective serotonin reuptake inhibitors
  • COC more for physical, not so much for mood symptoms
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16
Q

what is Polycystic ovary syndrome (PCOS)?

A
  • Ovaries produce an abnormal amount of androgens
  • Small cysts (fluid-filled sacs) form in ovaries
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17
Q

what is the clinical presentation of Polycystic ovary syndrome (PCOS)?

A
  • Menstrual irregularities
  • Androgen excess
    • Acne/ Hirustism/ Obesity
    • Metabolic disorders/ Insulin resistance —> DM, CVS disease
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18
Q

how to treat Polycystic ovary syndrome (PCOS)?

A
  • COC (can consider anti-androgenic progestin if acne/ hirsutism)
  • Metformin
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19
Q

What is menopause?

A

Permanent cessation of menses following the loss of ovarian follicular activity

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20
Q

how does menopause happen?

A
  • Natural
  • Induced: Removal of both ovaries or iatrogenic (illness due to treatment) ablation of ovarian function: Chemotherapy, pelvic radiation
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21
Q

whats the Clinical presentation for menopause?

A

note: DUE TO DECREASED ESTROGEN LEVELS

  • **Vasomotor symptoms: Several times a day due to thermoregulatory dysfunction which is triggered by a decreased estrogen, starting in the hypothalamus
    • Intense feeling of heat on face
    • Rapid or irregular heart rate
    • Flushing
    • Perspiration, Cold sweats
    • Sleep disturbances
    • Feeling of anxiety
  • Genitourinary syndrome
    • Changes to labia, clitoris, vestibule, vagina, urethra, bladder due to decreased estrogen
    • Genital dryness
    • Burning/ irritation/ pain
    • Sexual symptoms of lubrication difficulty
    • Impaired sexual function/ libido/ painful intercourse
    • Urinary urgency
    • Dysuria (painful urination)
    • Recurrent UTI
  • Psychological/ Cognitive
    • Likely multi-factorial (stress/ hormonal fluctuations)
    • Depression/ anxiety
    • Poor concentration/ memory
    • Mood swings
  • Bone fragility
    • Decreased estrogen —> More bone loss
    • Increased risk of osteoporosis and fractures
    • Increased joint pain
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22
Q

whats the Non-pharmacology for menopause?

A
  • For mild vasomotor symptoms
    • Layered clothing that can be removed or added as necessary to adapt to temp fluctuations
    • Lower room temp
    • Less spicy food/ caffeine/ hot drinks
    • More exercise
    • Dietary supplements (but conflicting results)
      • Isoflavones (phytoestrogen): Soybean, Leumes (lentils, chick pea)
      • Black cohost (herb): Serotonergic (serotonin) activity at hypothalamus
  • For mild vulvovaginal symptoms
    • Nonhormonal vaginal lubricants/ moisturizers
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23
Q

whats the pharma for menopause?

A
  1. Menopausal hormone therapy
  2. antidepressants
  3. gabapentin
  4. tibolone
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24
Q

what is Menopausal hormone therapy for in menopause?

A

Reserved for moderate/ severe symptoms or insuff response to nonpharma

  • Dont use this solely for
    • Treatment of low libido
    • CVD prevention
    • Depression/ anxiety/ cognitive/ memory issues
    • Itchy skin/ hair loss
    • Treatment of osteoporosis
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25
Q

is Menopausal hormone therapy the gold standard for menopause?

A

yes!!! GOLD

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26
Q

how does Menopausal hormone therapy work for menopause?

A

Increases Estrogen

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27
Q

what are the types of Menopausal hormone therapy for menopause?

A
  1. Estrogen only (unopposed estrogen)
  2. Estrogen + Progestin
    - Progestin addition
    • If have intact uterus: To protect endometrium from overgrowth and reduce risk of endometrial cancer
    • May improve vasomotor symptoms (VMS)
    • Dydrogesterone, norethisterone, medroxyprogesterone, micronized progesterone, norgestrel, levonorgestrel, gestodene, desogestrel, norgestimate
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28
Q

what are the sub types of Estrogen + Progestin under Menopausal hormone therapy for menopause?

A
  • Continuous-combined
    • Estrogen and progestin daily
    • No withdrawal bleeding although chance of breakthrough bleeding initially
    • After several months: Possible amenorrhea
  • Continuous-cyclic
    • Progestin added on either 1st or 15th of month, for 10-15 days
    • Withdrawal bleeding when progestin stopped
    • Regulate menses, which allows for predictable bleeding
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29
Q

how does menopausal hormone therapy compare with coc in terms of Physiologic goal?

A

mht: Replace/ supplement endogenous estrogen to alleviate symptoms and risks of lower estrogen production

coc: Suppress hypothalamus-pituitary-ovarian axis to avoid ovulation

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30
Q

how does menopausal hormone therapy compare with coc in terms of Amount of ethinyl-estradiol equivalents?

A

mht: 10-15mcg

coc: 20-50mcg

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31
Q

how does menopausal hormone therapy compare with coc in terms of Common formulations of estrogen used?

A

mht:
- 17 beta estradiol
- Conjugated equine estrogens (CEE)

coc:
- Ethinylestradiol
- Estradiol

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32
Q

why are systemic oral tablets for menopausal hormone therapy good and yet bad?

A

good: Cheaper

BAD:
- Higher dose required —> Higher risk of side effects
- Potential for missed dose —> Irregular bleeding

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33
Q

why are Systemic Topicals (Patches, Gels) for menopausal hormone therapy good and yet bad?

A

good:
- Lower systemic dose than oral
- Convi
- Continuous estrogen release

BAD:
- Expensive
- Skin irritation (rotating sites helps)
- Gel has more variability in absorption

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34
Q

why are Local vaginal (Pessary, Creams) for menopausal hormone therapy good and yet bad?

A

good:
- Lowest estrogen dose —> No need concomitant progestin
- Continuous estrogen release

BAD:
- Inconvi/ uncomfortable
- Vaginal discharge
- Only for localised urogenital atrophy

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35
Q

what are the risks associated with mht?

A
  • Breast cancer
  • Endometrial cancer
  • Venous thromboembolism
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36
Q

how to monitor if use mht?

A
  • 2-3 months of use before improvement with symptoms
  • Continue MHT if there is a need
  • Upon initiation
    • Annual mammography
    • Endometrial surveillance
      • Unopposed estrogen: Vaginal bleeding
      • Continuous-cyclic: Bleeding occurs when progestin is still on
      • Continuous-combined: Prolonged bleeding, heavier than normal, frequent, persists after >10 months of usage
  • Upon discontinuation
    • 50% chance of symptoms returning
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37
Q

what are the diff types of antidepressants one can use for menopause?

A
  • Serotonin and norepinephrine reuptake inhibitors
    • Venlafaxine
  • Selective serotonin reuptake inhibitors
    • Paroxetine
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38
Q

how can Gabapentin help with menopause?

A

Helps with night sweating and sleep disturbances

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39
Q

what is tibolone?

A

Synthetic steroid with estrogenic, progestogenic, androgenic effects

costly

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40
Q

how can tibolone help with menopause?

A
  • Improves mood, libido, menopause symptoms, vaginal atrophy (less than estrogen)
  • Protects against bone loss
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41
Q

who is tibolone for?

A

Only for postmenopausal women more or equal to 12 months since last natural period

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42
Q

what risks is tibolone associated with?

A

Risk of stroke, breast CA recurrence, endometrial cancer

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43
Q

best treatment for severe vasomotor symptoms of menopause

A

MHT

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44
Q

what is Hypertension in Pregnancy?

A

One of the most common causes of mortality in pregnancy

  • Based upon >1 measurement min 4h apart
    • SBP >140mmHg or DBP >90mmHg
  • Severe Hypertension, based upon 2 measurements
    • SBP >160mmHg and/or DBP >110mmHg
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45
Q

what are the Categories for htn in preggos?

A
  • Chronic Hypertension
    • Before 20 weeks gestation: Pre-existing or new onset hypertension
    • No proteinuria (albuminuria: elevated levels of proteins)
  • Gestational Hypertension
    • After 20 weeks of gestation: New onset hypertension
    • No proteinuria
  • Pre-eclampsia
    • After 20 weeks of gestation: New onset hypertension AND new onset of (either one?????)
      • Proteinuria
        • 24h urinary protein (UTP) >300mg
          • normal is <150mg/day
        • Dipstick protein >2
        • Urine protein: Creatinine ratio (uPCR) >0.3mg/dL
      • Signs of end-organ dysfunction
        • Platelet count <100 —> Clotting factors so bleeding complications
        • Liver Function Tests >2x ULN
        • Doubling of SCr in absence of other renal disease
        • Pulmonary edema (accumulation of fluids in lungs) —> SOB
        • Neurological complications
      • Uteroplacental dysfunction
  • Chronic Hypertension with superimposed pre-eclampsia
    • Superimposed: Secondary infection that occurs during an existing infection, or immediately following a previous infection.
    • Before 20 weeks gestation: New onset proteinuria
    • No proteinuria previously
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46
Q

what is Eclampsia?

A

MEDICAL EMERGENCY: Risk for both maternal and fetal

  • Sudden onset of seizures, which can be tonic-clonic (involve whole body), focal (affect specific part) or multifocal superimposed on pre-eclampsia
  • Pre-eclampsia can progress rapidly to eclampsia
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47
Q

what are the symptoms of eclampsia?

A
  • N/v
  • Palpitation
  • Flushing
  • Headache
  • Tremor
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48
Q

how to prevent pre-eclampsia?

A
  • Low dose 100mg or more aspirin
  • Start after 12 weeks, ideally before 16 weeks, continue till delivery
  • Reco for high risk patients: Hypertension on prev preggo, multifetal gestation, autoimmune disease, DM, CKD
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49
Q

what is the Pharmacology for hypertension in preggos?

A
  1. Methyldopa
  2. Labetalol
  3. Calcium channel blocker: Nifedipine ER
  4. Hydrochlorothiazide
  5. Hydralazine
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50
Q

why does methyldopa suck in treating htn in preggos?

A
  • Low potency
  • Increase ADR (sedation, dizziness)
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51
Q

which are the most commonly used drugs for htn in preggos?

A
  1. Labetalol
  • Preferred over other beta blockers because less ADR on uteroplacental blood flow and fetal growth
  • Bronchoconstrictive effects, bradycardia
  1. Calcium channel blocker: Nifedipine ER
  • Monitor for pedal edema (fluid gathers in feet), flushing, headaches
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52
Q

whats the 2nd or 3rd line drug for htn in preggos?

A

Hydrochlorothiazide

but note Potential interference with normal blood volume expansion during preggo

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53
Q

what to watch out for when taking hydralazine for htn in pregos?

A

ADR mimics symptoms assoc with severe preeclampsia and imminent eclampsia

54
Q

When to initiate treatmen for htn in pregs?

A
  • 140/90mmHg
  • Used to be >160/110mmHg (severe chronic hypertension)
55
Q

what are the Non-hormonal contraceptives: Barrier techniques?

A
  1. Male condoms (external)
  2. Female condoms (internal)
  3. Diaphragm with spermicide
  4. Cervical cap
56
Q

what are the contraindicates for the following?

A
  1. Male condoms (external)
    - Latex or rubber allergy
  2. Female condoms (internal)
    - Polyurethane allergy
    - History of toxic shock syndrome (TSS)
  3. Diaphragm with spermicide
  4. Cervical cap
    - Latex or rubber or spermicide allergy
    - Recurrent UTIs
    - History of TSS
    - Abnormal gynaecological anatomy
57
Q

what are the adv for the following Non-hormonal contraceptives: Barrier techniques?

A
  1. Male condoms (external)
    - STI protection
  2. Female condoms (internal)
    - Can be inserted ahead of time
    - STI protection
  3. Diaphragm with spermicide
  4. Cervical cap
    - Low cost
    - Reusable
58
Q

what are the disadv for the following Non-hormonal contraceptives: Barrier techniques?

A
  1. Male condoms (external)
    - High user failure rate
    - Poor acceptance
    - Possibility of breakage
  2. Female condoms (internal)
    - Very High user failure rate
    - Dislike ring hanging outside vagina
  3. Diaphragm with spermicide
  4. Cervical cap
    - High user failure rate
    - Low protection against STIs
    - Increased risk of UTI
    - Cervical irritation
59
Q

what are the Hormonal contraceptives avail?

A
  1. Oral contraceptives
  2. Transdermal contraceptives
  3. Long acting injections: Progestin injections
  4. Long acting reversible contraception
60
Q

what is hormonal contraceptives?

A

Combination of progestin and/or estrogen

61
Q

what are the hormonal Oral contraceptives avail?

A
  1. Combined Oral Contraceptives (COC)
  2. Progesterone Only Pill (POP)
62
Q

how does progestin work ?

A

Block LH surge —> Prevents ovulation

63
Q

whats the goals of the usage of progestin?

A

Thickens cervical mucus to prevent sperm penetration, slows down tubal motility (delay sperm transport), induce endometrial atrophy

Provide most of contraceptive effect

64
Q

what kind of activity does progestin have? and what are the side effects if any?

A
  • Has progestational activity and inherent androgenic effects
    • 😖Androgenic ADR: Acne, oil skin, hirsutism (excess hair on certain parts)
65
Q

what is a type of progestin?

A
  • Drospirenone (4th gen)
    • Analogue of spironolactone
    • Goals: Anti-mineralcorticoid, some anti-androgenic action
    • Less water retention, less acne
    • 😖ADR: Hyperkalemia, thromboembolism, bone loss

note: Cyproterone no longer used for birth control

66
Q

whats the goals of using estrogen ?

A

Stabilise endometrial lining and provide cycle control

67
Q

how does estrogen work?

A

Suppress FSH release —> Prevents ovulation

68
Q

what are the types of estrogen?

A
  • Ethinyl estradiol*
  • Estradiol valerate
  • Esterol
  • Mestranol
69
Q

whats the dosing for estrogen?

A
  • Low dose: 15-25mcg
    • For adolescence, <50kg, >35yo, peri-menopausal, fewer side effects
  • Mod dose: 30-35mcg
    • For >70.5kg, early to mid cycle breakthrough bleeding/ spotting or non-adherence
  • High dose: >50 mcg
70
Q

whats the types of COC based on content?

A
  • Monophasic COC: Same amounts of estrogen and progestin in every pill
    • Less confusing, less complicated missed dose
  • Multiphase COC: Variable amounts of estrogen and progestin
    • Lower progestin overall —> Lesser side effects
71
Q

whats the Types of COC based on duration of treatment?

A

note: Placebo: Pill-free or placebo to allow for withdrawal bleed before starting a new pack if it’s a cycle

  • Conventional-cycle COC
    • 21d active pill+ 7d placebo = 28d
    • Newer formulations: 24d active pill + 4d placebo = 28d
      • Shorter pill-free interval to reduce hormone fluctuations between cycles —> Less SE
  • Extended-cycle COC
    • 84d + 7d placebo = 91d
    • Convi, lesser periods
  • Continuous COC
    • Just keep taking, no placebo
    • Convi, lesser periods
72
Q

How to initiate a COC?

A
  • First day method
    • Start on first day of menstrual cycle
    • No backup contraceptive required if on first day cos you stop the process before it starts
    • Immediate protection against pregnancy
  • Sunday start
    • Start on first sunday after menstrual cycle begins
    • Require backup contraceptive (eg. male condoms) for at least 7d
    • May provide weekends free of menstrual periods
  • Quick start
    • Start now
    • Require backup contraceptive for at least 7d and potentially till next menstrual cycle begins
73
Q

what are the Factors to consider when selecting COC?

A
  • Hormonal content required
  • Convenience
  • Adherence level
  • Tendency for oily skin, acne, hirsutism —> COC has side health benefits
  • Medical conditions (eg. premenstrual syndrome, dysmenorrhea)
74
Q

what are the Bonus of other health benefits when using coc?

A
  • Menstrual benefits
    • Improve menstrual cycle regularity
    • Relief from menstrual related problems
  • Management
    • Peri-menopause, Polycystic ovary syndrome (PCOS), Iron-deficient anemia due to reduction of bleeding, Premenstrual dysphoric (dissatisfied) disorder by regulating hormones, Acne
  • Reduction of risk
    • Ovarian and endometrial cancers, ovarian cysts, ectopic preggo, pelvic inflam diseases, endometriosis, uterine fibroids, benign breast disease
75
Q

whats the adrs for coc?

A
  1. breast cancer
  2. venous thromboembolism
    - Estrogens: Increase hepatic production of factor VII, X and fibrinogen of coagulation cascade
    - New gen progestins (drosperinone, cyproterone, desogestrel)
  3. Ischemic stroke/ Myocardial infarction
76
Q

when to avoid using coc?

A

if have risk factors for the following:

  1. Breast cancer
    - Avoid if FH or risk factors of breast cancer, >40 years old, current history/ recent (within 5y)
    - Risk increases with duration and age >40
    - Risk removed upon discontinuation
  2. Venous thromboembolism
    - risk factors: >35yo, obesity, smoker, immobilization, cancer, hereditary thrombophilia
  3. Ischemic stroke/ Myocardial infarction
    - risk factors: Age, hypertension, obesity, dyslipidemia, smoking, prothrombotic mutations —> Consider low dose estrogen/ progestin-only/ barrier instead
    - contraindications: Migraine with aura (recurring headache that strikes with sensory disturbances called aura)
77
Q

what to consider instead of coc if have risk factors for the following:

A
  1. risk factors for Venous thromboembolism
    - Consider
    • Low dose estrogen with older progestins
    • Progestin-only contraceptive
    • Barrier methods
  2. risk factors for ischemic stroke/ mi
    - Consider low dose estrogen/ progestin-only/ barrier instead
  3. risk factors of ischemic stroke/ mi and migraine with aura
    - Consider progestin-only/ barrier instead
78
Q

what are the contraindications for coc?

A
  • Current/ recent history (within 5y) breast CA
  • History of venous thromboembolism or pulmonary embolism and/or on anticoagulent therapy
  • Major surgery with prolonged imobilization
  • <21d postpartum with other risk factor
  • <6weeks postpartum if breastfeeding
  • Thrombogenic mutations
  • Systemic Lupus Erythematosus and/or Antiphospholipid Syndrome
  • Migraine with aura
  • SBP > 160mmHg / DBP > 100mmHg
  • Hypertension with vascular disease
  • Current/ history of ischemia heart disease
  • Cardiomyopathy
  • Smoking >15 sticks/d AND age >35yo
  • History of cerebrovascular disease
  • Diabetes >20y or with complications
79
Q

when do adr for coc occur?

A

Normally occurs during early COC use, may improve by 3rd-4th cycle after adjusting to hormone levels

Counsel to ensure continued adherence on COC for 2-3 months before changing products UNLESS vv serious ADR like VTE/ stroke/ migraine with aura/ MI

80
Q

how to manage adr (Breakthrough bleeding) for coc?

A
  • If early/ mid cycle: Increase estrogen
  • If late cycle: Increase progestin
81
Q

how to manage adr (menstrual cramps) for coc?

A
  • Increase progestin/ switch to extended cycle or continuous
82
Q

how to manage adr (acne) for coc?

A
  • Change to less androgenic progestin
  • Consider increasing estrogen: If on POP, change to COC
83
Q

how to manage adr (bloating) for coc?

A
  • Reduce estrogen
  • Change to progestin with mild diuretic effect: Drospirenone
84
Q

how to manage adr (n/v) for coc?

A
  • Reduce estrogen
  • Take pills at night/ change to POP
85
Q

how to manage adr (Headache) for coc?

A
  • Exclude migraine with aura first
  • Usually occurs in pill-free week —> Switch to extended cycle/ continuous/ shorter pill-free interval
86
Q

how to manage adr (Breast tenderness/ weight gain) for coc?

A
  • Keep both estrogen/ progestin as low as possible
87
Q

whats the ddi to take note of for coc?

A

note: Lower the dose of hormone in COC, greater risk of DDI —> Lesser efficacy

  1. Rifampin (antibiotic)
  2. anticonvulsants
  3. hiv antiretrovirals
88
Q

how does rifampin affect coc? (ddi)

A
  • Alters gut flora —> Alter metabolism —> Less active drug
  • Use additional contraception till rifampin discontinued for at least 7 days
89
Q

how does Anticonvulsants affect coc? (ddi)

A
  • Reduces free serum conc of both estrogens and progestin
  • Phenytoin, carbamazepine, barbiturates, topiramate, oxcarbazepine, lamotrigine
90
Q

how does HIV antiretrovirals affect coc? (ddi)

A
  • Reduces both effectiveness of COC and antiretrovirals
  • Protease inhibitors: Ritonavir, darunavir
91
Q

what happens if miss dose of coc?

A
  1. Miss one dose (within 48h)
    - Take missed dose immediately and continue the rest as usual —> So take the next pill as if never miss the prev one
    - No need additional contraceptive
  2. Miss two or more consec doses (>48h)
    - Take missed dose immediately and discard rest of missed dose
    - Continue rest as usual as if never miss prev dose
    - Backup contraceptive required for at least 1 week
  3. Miss dose during last week of cycle
    - Finish remaining active pills in current pack
    - SKIP hormone-free interval and start new pack the next day
    - Backup contraceptive for at least 7d
92
Q

what is pop for?

A

Good for breast feeding, intolerant to estrogen (eg. n/v), conditions that preclude (rule out) estrogen

93
Q

what is the failure rate for pop?

A

Typical use failure rate 7% (same as COC)

94
Q

when to NOT use pop?

A

AVOID if breast cancer

95
Q

what are the diff types of pop?

A
  • Norethindrone or Levonorgestrel
    • 28 active pills (continuous)
  • Drospirenone
    • 24 active pills, 4 inactive
96
Q

when to start treatment for pop?

A
  • Within 5d of menstrual cycle —> No need backup
  • Any other day —> Backup contraceptive for 2d (7d for drospirenone)
97
Q

what happen if miss dose for pop?

A
  • N/L: If miss by >3h, take extra and continue + backup for 2d
  • Drospirenone: If <24h, take extra and continue. If >2 active pills missed, backup needed for 7d
98
Q

what kind of transdermal contraceptives are there?

A
  1. patches
  2. vaginal rings

note: Continuous, higher exposure to estrogen —> Increased risk of VTE

99
Q

what is the failure rate for use of patches and vaginal rings as contraceptives?

A

Typical use failure rate 7% (same as COC)

100
Q

what does patches and vaginal rings as contraceptives contain?

A

Contains estrogen and progestin

101
Q

who is patches as contraceptives reco to?

A

Reco for those <90kg

102
Q

how to apply patches as contraceptives?

A

Apply once weekly x3weeks, then 1 patch-free week

103
Q

when to discard vaginal rings?

A

Use for 3 weeks then discard

104
Q

how to put on vaginal rings?

A

Precise placement not an issue as hormones are absorbed (unlike diaphragms/ cervical caps)

105
Q

whats the failure rate for long acting progestin injections?

A

Typical use failure rate 4%

106
Q

what is a type of long acting progestin injections?

A
  • Depo-Provera
  • IM injection Q12h
107
Q

whats the thing about long acting progestin injections?

A
  • Good for adherence, but need visit doc regularly
  • Might delay return to fertility
108
Q

whats the adr for long acting progestin injections?

A
  • 😖ADR
    • Variable breakthrough bleeding esp first 9 months
      • Amenorrheic: 50% after 12m, 70% after 2y
    • Weight gain (more than other types!!)
    • BLACK BOX WARNING: Short term bone loss —> Bone mineral density decrease
      • Avoid in older women, osteoporosis risk factors (eg. long term steroids), >2y
109
Q

what is Long acting reversible contraception? and what are the two types?

A

Hormonal and non-hormonal contraceptives

  • Effects quickly reversible upon removal
  • Not commonly used due to invasiveness
  1. subdermal implants: progestin implants
  2. intrauterine devices (iud)
110
Q

whats the failure rate for Long acting reversible contraception?

A

Highly effective: Typical use rates, perfect-use rates <1%

111
Q

what is Subdermal implants: Progestin implants?

A
  • Single 4cm long implant
  • Contains 68mg of etonogestrel
  • Last 3 years
  • Irregular bleeding pattern with continued use: Amenorrhea*, prolonged bleeding, spotting**, frequent bleeding
112
Q

how does iud work?

A
  • MOA: Inhibit sperm migration, damage ovum, damage/disrupt transport of fertilized ovum
    • If have hormones like progestin: Endometrial suppression, thicken mucus
113
Q

when to avoid using iud?

A

AVOID inserting if preggo, current STI, undiagnosed vaginal bleeding, malignancy of genital tract, uterine anomalies, uterine fibroids

114
Q

whats the adr for iud?

A

😖ADR: Uterine perforation, expulsion, pelvic infection

115
Q

what are the two types of iud?

A
  1. levonorgestrel iud
  2. copper iud
116
Q

whats the diff between the two types of iud?

A
  1. levonorgestrel iud
    - leads to a Menstrual flow decreased
    - associated with Typical spotting, amenorrhea
    - 5 years
  2. copper iud
    - leads to Heavy menses
    - Ideal if concomitant amenorrhoea
    - 10y
    - can use as emergency contraception
117
Q

how to get access to emergency contraception?

A

Requires prescription

118
Q

what are the types of emergency contraception?

A
  • Copper IUD**
    most effecitve
    insert within 5d
    inhibits sperm migration, damage ovum, disrupt transport of fertilised ovum
  • Ella tablet
    1 tablet asap within 5d
    slows release of GnRH inhibiting ovulation
    thins uterine lining
  • Postinor 2 tablet (levonorgestrel 0.75mg)
    2 tabs asap within 12h
    slows release of GnRH inhibiting ovulation
    thins uterine lining
119
Q

what are the side effects of emergency contraception?

A
  • Side effect: Nausea with oral option
    • If vomits within 3h of taking tablet, redose!!!
120
Q

whats the female pharmaco for oral contraceptives?

A
  1. Ethinyl estradiol (synthetic estrogen)
  2. Norethindrone (synthetic progestogen)
121
Q

how does Ethinyl estradiol (synthetic estrogen) work?

A
  • Estrogen receptor agonist: Binds to estrogen receptors
  • Negatively regulates hypothalamic-pituitary-ovarian axis —> Inhibits follicle-stimulating hormone released from anterior pituitary —> Suppresses development of ovarian follicle —> Makes endometrium unsuitable for implantation of ovum
122
Q

what is Ethinyl estradiol (synthetic estrogen) for?

A
  • Menopausal symptoms (mood swings, body changes)
  • Gynecological disorders
  • Certain hormone-sensitive cancers
123
Q

whats the pkpd for Ethinyl estradiol (synthetic estrogen)?

A
  • A
    • Well absorbed orally (but also can be admin parental, transdermal, topical)
    • OD
    • Fast Onset 30-69mins
    • Good F = 0.45
  • D
    • Very highly plasma protein bound
  • M
    • Metabolised by liver
      • Phase 1: Hydroxylation by CYP3A4
      • Phase 2 (make more water soluble): Conjugation with glucuronide and sulfation —> Ethinylestradiol glucuronides and Ethinylestradiol sulfate
        • Both inert, so no estrogenic effect
    • t1/2 = 13-27h
      • Inert compounds can undergo enterohepatic recirculation from liver to bile to small intestine to be reabsorbed back to liver —> Long half life
  • E
    • Metabolites excreted in faeces and urine
124
Q

whats the adr for Ethinyl estradiol (synthetic estrogen)?

A
  • Breast tenderness
  • Headache
  • Fluid retention (bloating)
  • Nausea
  • Dizziness
  • Weight gain
  • Venous ThromboEmbolism (VTE) —> block blood vessel !!!
  • MI/ stroke
  • Liver damage
125
Q

who should not take Ethinyl estradiol (synthetic estrogen)?

A
  • Known history or susceptibility to arterial or venous thrombosis (because potential severe side effect)
  • Advanced diabetes with vascular disease
  • Hypertension >160/100
  • Avoid in breastfeeding <21d postpartum and breast cancer
126
Q

how does Norethindrone (synthetic progestogen) work?

A
  • Progesterone receptor agonist: Binds to progesterone receptors
  • Negatively regulates hypothalamic-pituitary-ovarian axis —> Inhibits luteinizing hormone released from anterior pituitary —> Prevents ovulation —> Makes endometrium unsuitable for implanation of ovum
127
Q

who is Norethindrone (synthetic progestogen) for?

A
  • Endometriosis (Tissue similar to uterus lining grows outside of uterus)
  • Abnormal periods or bleeding and to bring on a normal menstrual cycle
128
Q

whats the pkpd for Norethindrone (synthetic progestogen) ?

A
  • A
    • Well absorbed orally OD
    • Quick onset
    • Good bioavailability 64%
  • D
    • Highly plasma protein bound
  • M
    • Metabolised in liver by phase 1 reduction then phase 2 glucuronidation and sulfation
    • t1/2 = 8h
    • Some % of norethindrone can be metabolised in liver to EE
  • E
    • Metabolites excreted in urine and faeces
129
Q

whats the adr for Norethindrone (synthetic progestogen) ?

A
  • Headache
  • Dizziness
  • Bloating
  • Weight gain
  • Episodies of unpredictable spotting and bleeding
  • Amenorrhea (absence of periods)
130
Q

who is Norethindrone (synthetic progestogen) not desirable for?

A

Not desirable for women planning for pregnancy soon after cessation of therapy as ovulation suppression can persist for like 1.5y

131
Q

can Norethindrone (synthetic progestogen) convert to Estrogen? and if so what does this cause?

A

yes
Partial conversion of nonethindrone to EE may cause potential CVS complications of EE (eg. Venous thromboembolism)

finals (8 decks)

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