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Week 5 Flashcards

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1
Q

What does STRAW stand for? What is the definition of STRAW?

Does perimenopause last longer than menopausal?

What kind of symptoms do you get near menopause?

A

STRAW (STages of Reproductive Aging)

  • Definition: lays out phases of menstrual lifespan (reproductive, menopausal transition, and post-menopause
    • Perimenopause may last longer than menopausal transition (involves period before and after last menstrual period)
    • Vasomotor symptoms are most likely to occur in late menopausal transition and early post-menopause
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2
Q

Define mepopause and give epidemiology.

A

Menopause

  • Definition: the final menstrual period (FMP) confirmed after one year of no menstrual bleeding; permanent cessation of menses
  • Epidemiology: 51 to 52 y/o
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3
Q

What is the physiology of menopause?

A
  • Physiology:
    • Follicular and oocyte depletion as a women ages due to gene regulated apoptosis and ovulation
    • Decrease in estrogen → GnRH activation via feedback mechanism → constant release of LH and FSH → very high serum levels of LH/FSH (specific for menopause)
    • Decline in fertility: fertility is near its end at age 42
    • Granulosa cells of antral follicles produce AMH → can be used to determine the number of remaining follicles (declines in menopause)
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4
Q

What are the symptoms of menopause?

A
  • Symptoms:
    • Vasomotor symptoms (hot flashes and night sweats), vaginal atrophy, sleep disturbances, psych disturbances (moody attitude), decreased libido
      • Hot flashes: narrowing of thermoregulatory zone of brain → body is tricked into thinking the woman is “hot” → hot flashes (dilation of peripheral vessels)
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5
Q

What are the complications of menopause?

A
  • Complications of menopause
    • Decreased estrogen → increased LDL/total cholesterol → increased risk of CVD (number one cause of mortality in females age 50+)
    • Estrogen has an impact on insulin and glucose metabolism
    • Estrogen inhibits the activity of osteoclasts; therefore, in menopause, lack of estrogen is associated with osteoporosis
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6
Q

What are hormonal treatments of menopause?

A
  • Hormonal tx of hot flashes, vaginal atrophy, and decreased libido: estrogen + progesterone (prevents endometrial hyperplasia)
    • Estrogen promotes mucosal water retention, sebaceous gland secretion, and maintains blood flow, acidic pH, and elasticity of vagina
    • Lifestyle changes: exercise, keep cool, avoid hot flash triggers (spicy and hot foods), R-E-L-A-X
    • For decreased libido: testosterone can also be used
    • Contraindications of estrogen replacement therapy: ER+ breast cancer, hx of DVT/PE
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7
Q

Define perimenopause and provide epidemiology.

A

Perimenopause

  • Definition: transition phase from reproductive phase to post-menopausal phase; most symptomatic period in women’s life
    • Begins with varied menstrual cycle that can last >7 days
    • Characterized by unpredictable hormone concentrations
  • Epidemiology: 34 to 54 y/o lasting 5-6 years (avg: 46 y/o)
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8
Q

What are non hormonal treatments of menopause?

A
  • Nonhormonal prescriptions that act on CNS (directly on hypothalamus)
    • Hot flashes: antidepressants (SSRI/SNRI), hypnotic meds, anticonvulsants (Gabapentin), Antihypertensive (clonidine), neuropathic pain drugs
    • Vaginal atrophy: vaginal moisturizers (hydrophilic biofilms that cling to vaginal wall), sexual lubricants, estrogen
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9
Q

Define primary ovarian insufficiency and provide symptoms/presentation.

A

Primary Ovarian Insufficiency (aka premature menopause)

  • Definition: loss of ovarian function that occurs prior to age 40
    • Follicles are still present, but no longer functional
    • POI may not be permanent
  • Presentation: infertility, menstrual dysfunction, symptoms of estrogen deficiency, sexual dysfunction
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10
Q

For primary ovarian insufficiency, provide etiology, risk factors, and treatment.

A
  • Etiology: follicular dysfunction (90%), follicular depletion (10%)
  • Risk factor: Fragile X carrier status, thyroid dysfunction, adrenal dysfunction
  • Treatment: hormone replacement therapy to combat the risks of estrogen depletion
    • No treatment to induce ovulation in infertile females with POI, but there is a small chance for spontaneous pregnancy (no chance with menopause)
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11
Q

What are the two regions near the pituitary gland? What do they contain?

A
  • Regions
    • Sellar region: region that includes the pituitary gland
    • Parasellar region: regions that includes the optic chiasm and cranial nerves
  • Lesions and tumors can affect both regions
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12
Q

What are two types of pituitary adenomas? How do each present and how can they be treated generally?

A
  • Functioning vs non-functioning: functioning adenomas have hormonal secretions
    • Non-functioning pituitary tumors:
      • Present with compressive sx, hypopituitarism
      • Tx: transsphenoidal hypophysectomy followed w/ radiation
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13
Q

What are the cellular subtypes of pituitary adenomas? What are complications associated with pituitary adenoma?

A
  • Subtypes: PLH (prolactin hormone), ACTH, GTH, GH, and TSH
  • Complications of pituitary adenoma:
    • Hypopituitarism: typically hypersecretion of one hormone and hyposecretion of other hormones due to pituitary compression
    • Pituitary apoplexy: hemorrhage of pituitary gland
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14
Q

What are two size subtypes of pituitary adenoma and what are they associated with?

A
  • Size subtypes: Microadenoma (<1cm), macroadenoma (>1cm)
    • Microprolactinoma: no compressive symptoms
    • Macroprolactinoma: compressive symptoms (i.e. vision disturbances, facial drooping)
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15
Q

What are causes of hyperprolactinemia?

Divide between physiologic and pathologic

A
  • Causes of hyperprolactinemia:
    • Physiologic: pregnancy (estrogen increases prolactin levels), nipple stimulation, stress, exercise, chest trauma
    • Pathologic: decreased dopamine response (due to masses or psych drugs), renal failure (decreased peripheral clearance of prolactin), hypothyroidism (TRH causes increase in prolactin)
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16
Q

What are clinical manifestations of hyperprolactinemia and provide mechanism

A
  • Clinical manifestations
    • Galactorrhea, amenorrhea, decreased libido, headache (compression)
    • Increased prolactin → negative feedback on GnRH → decreased LH/FSH → decreased estrogen → infertility, sexual dysfunction, osteoporosis
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17
Q

How do you treat prolactinoma?

Provide side effects of drug! Provide a surgery too

A
  • Treatment of prolactinoma:
    • Dopamine agonist (first line treatment): bromocriptine, cabergoline
      • SE of bromocriptine: N/V, postural hypotension on first dose
    • Surgery: debulking procedure (if resistant to drugs), radiation therapy (if resistant to drugs/debulking)
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18
Q

What two things can a growth hormone cell adenoma cause? Describe the clinical manifestations of each!

A
  • Growth hormone cell adenoma
    • Types
      • Gigantism (child form):
        • Clinical presentation: increased linear bone growth in children (epiphyses are not fused)
      • Acromegaly (adult form):
        • Clinical manifestations: enlarged bones of hands/feet/jaw, growth of visceral organs (large heart → failure) enlarged tongue
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19
Q

How do you diagnose and treat growth hormone cell adenoma?

A
  • Diagnosis: elevated GH (lack of negative feedback by oral glucose) and IGF-1 (insulin growth factor)
  • Treatment: octeotride (somatostatin analog à inhibition of GH release), cabergoline (dopamine agonist), pegvisomant (GH receptor antagonist), surgical debulking, radiation treatment (for residual tumor post-surgery or failed drugs)
    • Goal is to keep GH < 1.0 ng/mL
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20
Q

Define hyppituitarism and proivde diagnostic labs.

A
  • Definition of hypopituitarism
    • Occurs when >75% of pituitary parenchyma is lost
  • Diagnostic labs of hypopituitarism:
    • Free T4, testosterone (men), AM cortisol, GH following insulin-induced hypoglycemia, electrolytes
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21
Q

What is the etiology of hypopituitarism? Provide a few syndromes and a lot of other diseases.

A
  • Etiology of hypopituitarism
    • Vascular disorders: pituitary infarction, pituitary apoplexy, aneurysm, vasculitis
      • Sheehan’s syndrome: in pregnancy, pituitary gland doubles in size, but blood supply does not increase → pituitary infarction
      • Empty cell syndrome: congenital defect of sellar region
        • Pathophysiology: herniation of arachnoid and CSF into sellar region → compression → destruction of pituitary gland → empty cell syndrome
    • Physical agents: radiation, surgery, head trauma
    • CNS insults: meningitis
    • Inflammatory/granulomatous diseases: TB, sarcoidosis, histiocytosis, hemochromatosis, hypophysitis
    • Idiopathic: GH deficiency, hypogonadotropic hypogonadism
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22
Q

What is the etiology, sx, and tx of central diabetes insipidus?

A
  • Diabetes insipidus
    • Central (ADH deficiency)
      • Etiology: all causes of hypopituitarism
      • Sx: polydipsia, polyuria, life-threatening dehydration
      • Tx: desmopressin (ADH analog), water, treat underlying cause
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23
Q

What is the etiology of nephrogenic diabetes insipidus?

A
  • Nephrogenic (ADH resistance)
    • Etiology: familial, metabolic (low Ca, high K, lithium, osmotic diuresis, chronic renal disease
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24
Q

For the following conditions, provide urine volume, urine osmolarity, serum osmolarity, respose to dehydration, response to exogenous ADH:

  • Central DI
  • Nephrogenic DI
  • Fluid overload
A
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25
# Define unintended pregnancy, how many in US are unintended, epidemiology. What are the two most common contraceptives?
* Unintended pregnancy: defined as a pregnancy that is either unwanted, unplanned, or simply mistimed * ~50% of pregnancies in the United States are unintended (more than other developed countries) * Epidemiology: teenagers, unmarried women, black women, sexual minorities, low education/income * Most common contraceptives: tubal ligation, oral contraceptive pill
26
What are some barriers to effective contraception?
* Barriers to effective contraception: * Physical ability to use methods, religious contraindications, cost, accessibility, insurance coverage, medical contraindications
27
Provide the MOA of the two hormones involved in contraceptives?
* Progestin (prevents ovulation and fertilization) * Suppresses LH surge, thickens cervical mucus, reduces ovum motility, thins endometrium * Estrogen * Suppresses FSH, potentiates progestin
28
Provide the following generally: * half-life of each hormone * where are they metabolized * which two drugs do not have a rapid return to fertility? * what is the effect on obese patients? * What are general side effects of all?
* General pharmacokinetics/pharmacology * Half-life: estrogen (long), progestin (short * Metabolism: liver (P450s) * Return to fertility: rapid except for depo (9-10 months) and Nexplanon (1-2 months) * Effect in obese patients: Nexplanon and OCPs may be slightly less effective (others are equally effective) * General side effects: all can cause spotting of blood except copper IUD (can cause heavy bleeding)
29
For Emergency contraception (Plan B/levonorgestrel): * MOA * Benefits * Risks
30
For Fertility awareness methods (calendar, temperature, cervical mucus): * MOA * Benefits * Risks
31
For Barrier methods (condom, cervical cap, diaphragm): * MOA * Benefits * Risks
32
For Progestin only pills (POP): * MOA * Benefits * Risks
33
For Combined hormonal methods (oral contraceptive pill, ring, patch): * MOA * Benefits * Risks
34
For Depot medroxyprogesterone acetate (aka Depo-provera): * MOA * Benefits * Risks
35
For Levonorgestrel implant (nexplanon): * MOA * Benefits * Risks
36
For Copper IUD (ParaGard): * MOA * Benefits * Risks
37
For Levonorgestrel (LNG) intrauterine device (IUD) (mirena, Skyla, kyleena): * MOA * Benefits * Risks
38
For Surgical sterilization (vasectomy, tubal ligation, Essure): * MOA * Benefits * Risks
39
What are the phases of growth from pre natal to adult and what are the main factors that influence growth at each stage?
* Phases of growth: prenatal → infancy (nutrition) → childhood (growth hormone) → adolescence (growth hormone and sex steroids)
40
What are the maternal factors before and after pregnancy that affect prenatal growth of a baby?
* Prenatal growth * Maternal factors * Before pregnancy: maternal weight, nutritional status (folate deficiency) * During pregnancy: poor weight gain, chronic illness (malabsorption/DM/renal disease), poor nutrition, drug use, decreased O2 available to fetus (high altitude, anemia)
41
What are the fetal factors that affect prenatal growth of a baby?
* Fetal factors * Familial/chromosomal abnormalities, intrauterine infections (i.e. TORCH – most common infections associated with congenital abnormalities)
42
What are the uterine/placental factors that affect prenatal growth of a baby?
* Uterine/placental factors * Inadequate placental growth, uterine malformations, decreased utero-placental blood flow, multiple gestations
43
For intrauterine growth restriction, provide the definition, epidemiology, and co-morbidities (and why this happens)?
* Intrauterine growth retardation (IUGR) * Definition: combination of maternal and fetal factors that lead to a fetal weight of less than 10th percentile * Epidemiology: 20% of stillborn births, higher mortality rates * Co-morbidities: * Pathophysiology: decreased placental transfer of nutrients/oxygen → * Hypoglycemia, hypocalcemia, polycythemia, perinatal asphyxia, hypothermia (low fat storage), thrombocytopenia/leukopenia
44
What are the lasting effects of small birth size via IUGR?
* IUGR can lasting effects into adulthood: * Small birth size → abnormal glucose/insulin metabolism → increased risk of CVD, diabetes, cognitive disabilities, obesity, and cancers
45
Provide what normal weight gain, normal height gain, and normal growth velocity is?
* Normal growth patterns * Normal weight gain: babies double birth weight by four months, triple birth weight by one year, ~5 lbs weight gain/per inch height gain * Normal height gain: half of adult height achieved at 24-30 months, slump in height velocity right before pubertal growth spurt * Normal growth velocity (rule of fives): 0-1 yr (25cm/yr), 1-4 yrs (10cm/yr), 4 to puberty (5 cm/yr), puberty to adult (10-15cm/yr)
46
How is bone age determined? What bone parts are assessed?
* Bone age: generally use x-ray of left hand → assess epiphysis carpal bones → bone age and predicted adult height
47
When should you be worried about growth?
* Abnormal growth patterns * When to worry: height \< 3rd percentile, \> 97th percentile OR growth velocity \< 10th percentile, \>95th percentile
48
Provide etiologies of short stature (one big syndrome with sx and tx)?
* Short stature * Intrinsic short stature * Familial short stature * Turner Syndrome (45 X, null): short stature, primary amenorrhea, web neck, poor breast development, coarctation of aorta * Tx: estrogen * Delayed growth: undernutrition, chronic disease * Attenuated growth: malnutrition, severe chronic diseases, GI disease, metabolic/endocrine disease (hypothyroidism, Cushing’s) * Constitutional delay of growth (late bloomer): normal growth velocity, delayed skeletal maturity, delayed puberty, normal final height
49
Provide etiologies of tall stature divided between childhood and adult
* Tall stature * Childhood (normal adult height) * Exogenous obesity, precocious puberty, hyperthyroidism * Adult * Familial tall stature, excess GH secretion, androgen/estrogen deficiency, Klinefelter syndrome (XXY), XYY, Marfan syndrome
50
For the following diseases provide the trend of the height velocity, weight gain, and any other info: * Undernutrition * Hypothyroidism * Growth hormone deficiency * Cushing's * Turner Syndrome * Overnutrition * Klienfelter
51
Define puberty and provide 4 different events in females and males that occur.
* Puberty: transition from childhood to sexual maturity * General physiologic events: * Gonadarche: activation of gonads by GnRH → LH/FSH * Adrenarche: increase in androgen synthesis by adrenal cortex → stimulates hair, acne, and body odor * Spermarche: first sperm production * Pubarche: appearance of pubic hair
52
What is the general puberty timing in males and females? Provide the order of devleopment of different organs.
* Puberty timing (can change based on ethnicity) * Male: onset is 9-14 y/o * Gonadarche (testicular growth) → adrenarche → phallic growth → growth spurt (later than females) * Female: onset is 8-13 y/o * Thelarche (breast development) → adrenarche → growth spurt → menarche
53
How is GnRH released in pre-puberty when compared to puberty. How are the pre-puberty release of GnRH activated and inhbitied? What are physiological changes during puberty in hormones?
* Pre-puberty: low and infrequent GnRH pulses * Suppression due to: GABA, MKRN3 * Activation due to: glutamate, leptin, kisspeptin, neurokinin B * Puberty: increased frequency of GnRH pulses * Physiological changes: development of zona reticularis of adrenal glands → increase in DHEAS, androstenedione, and testosterone
54
What are pubertal changes associated with estrogen in a female? Explain the associated tanner changes here.
* Estrogen → growth spurt, body weight composition, bone growth, genital maturity, and breast development * Tanner Stages for breast * I (pre-pubertal): no breast tissue or changes * II-IV (pubertal changes): breast bud starts to develop and areola starts to separate from the nipple * V (mature stage): fully developed
55
What are pubertal changes associated with androgens in a female? Explain the associated tanner changes here.
* Androgens → pubic hair * Tanner Stages for pubic hair (true for males as well) * I (pre-pubertal): no hair * II-IV (pubertal changes): transformation from minimal hair to hair all around genitalia * V (adult appearance): hair from thigh to thigh
56
What are pubertal changes associated with testosterone in a male? Explain the associated tanner changes here.
* Male * Testosterone → growth spurt, testicular size, spermarche, and genitalia development * Tanner stages for genitalia * I – prepubertal * II – enlargement of testes and scrotum, scrotal skin reddens/texture change * III – penis enlarges (length 1st), testes grow * IV – increase in width, development of glans, testes & scrotum larger, scrotal skin darker * V – adult genitalia
57
Define precocious puberty and the age
* Precocious puberty: early sexual maturation (\< 9 y/o for boys, \< 8 y/o for girls)
58
How does central precocious puberty work and how is it treated?
* Central: GnRH-dependent sex hormone production → FSH/LH secretion is normal → results in iso-sexual sequential maturation (females → females) * Treatment: decide if needed
59
How does peripheral precocious puberty work? Give some etiologies. Give overall tx
* Peripheral: GnRH-independent sex hormone production → FSH/LH suppressed → results in iso-sexual or contrasexual (male develops as female) maturation * Etiology: Genetic (CAH, LH-R activating mutations, DAX1 gene mutations, McCune Albright syndrome) and tumors (adrenal, pituitary, ovarian, testicular) * Treatment: treat underlying disorders
60
What is McCune Albright syndrome? What signs are associated with it? What does it cause?
* McCune Albright syndrome: precocious puberty due to recurrent ovarian cysts and intermittent estrogen secretion * Signs: Café-au-lait skin lesions (coffee w/milk color), polyostotic fibrous dysplasia (lytic lesions in the bones) * CAUSES PERIPHERAL PRECOCIOUS PUBERTY
61
For benign premature thelarche, provide: * description * etiology * red flags * diagnosis
* Benign premature thelarche * Description: unilateral or bilateral breast development before the age of 2 with no other signs of puberty → regresses by age 2-3 y/o * Etiology: environmental * Red flags: lack of regression by age 3, breast d/c, other signs of puberty * Diagnosis: bone age, LH/FSH, estradiol, imaging (head)
62
What are the ages for delayed puberty in each gender?
* Delayed puberty (\>13 y/o for girls, \>14 y/o for males)
63
What are examples of the following: * Constitutional * Delayed, but spontaneous
* Constitutional delay (majority, especially in males) * Delayed, but spontaneous (functional hypogonadotropic hypogonadism) * Due to chronic disease, but normal HPG axis * Examples: Inflammatory disease, malnutrition, exercise, hypothyroidism, prolactinoma, craniopharyngioma
64
What are examples of the following: * Hypogonadotropic hypogonadism (one syndrome, provide pathophys, sx and tx)
* Hypogonadotropic hypogonadism * Ex: Kallmann syndrome – GnRH containing neurons failed to migrate from the olfactory placode to hypothalamus → lack of hormonal stimulation → no puberty * Symptoms: anosmia (dx: test olfaction) * Treatment: exogenous hormones
65
For hypergonadotropic hypogonadism, provide description, labs, and etiology
* Hypergonadotropic hypogonadism * Description: results of gonadal failure, intact HPG axis * Labs: elevated FSH * Etiology: Turner syndrome, Klinefelter syndrome, irradiation, chemotherapy, infection (dx: karyotype)
66
Provide two examples of unclassified delayed puberty
* Unclassified (anatomical abnormalities) * Mullerian agenesis (Mayer-Rokitansku-Küster-Hauser syndrome (MRKH) * Most common cause of primary amenorrhea because of absence of vagina, uterus and fallopian tubes; ovarian function is normal * Imperforate hymen, transeverse vaginal septum
67
Situations for elective and medically induced abortions?
* Elective: unintended pregnancy, domestic issues * Medically-indicated: risk to mother’s life, ectopic pregnancy
68
Two meds for medication induced abortion? Provide MOA and SE if any? When are these indicated?
* Medication-induced abortion (indicated up to 70 days with ~70% success) * Prostaglandin E1 analog – Misoprostol (given at very high dose on day 2) * MOA: cervical ripening and uterine contractions * SE: severe cramping, heavy bleeding * Antiprogesterone – Mifepristone (given day 1) * MOA: lack of progesterone à lack of uterine maintenance à abortion
69
Provide surgical methods to abort a baby? Provide MOA and inidcations. When is a baby viable?
* Surgery (indicated after 70 days to end of first trimester) * MOA: suction, dilation, and evacuation à abortion * Viability starts ~24 weeks, so many states will not abort during the second trimester onwards
70
What are the provider roles in abortion?
* Understand that it is the patient’s decision and that it is difficult concept * You must manage complications (death of mother), review obstetric history, and manage psychological impact of the abortion on the patient

EndoRepro (8 decks)

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