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EndoRepro > Week 5 > Flashcards

Week 5 Flashcards

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
Q

Define unintended pregnancy, how many in US are unintended, epidemiology.

What are the two most common contraceptives?

A
  • 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
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26
Q

What are some barriers to effective contraception?

A
  • Barriers to effective contraception:
    • Physical ability to use methods, religious contraindications, cost, accessibility, insurance coverage, medical contraindications
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27
Q

Provide the MOA of the two hormones involved in contraceptives?

A
  • Progestin (prevents ovulation and fertilization)
    • Suppresses LH surge, thickens cervical mucus, reduces ovum motility, thins endometrium
  • Estrogen
    • Suppresses FSH, potentiates progestin
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28
Q

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?
A
  • 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)
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29
Q

For Emergency contraception (Plan B/levonorgestrel):

  • MOA
  • Benefits
  • Risks
A
30
Q

For Fertility awareness methods (calendar, temperature, cervical mucus):

  • MOA
  • Benefits
  • Risks
A
31
Q

For Barrier methods (condom, cervical cap, diaphragm):

  • MOA
  • Benefits
  • Risks
A
32
Q

For Progestin only pills (POP):

  • MOA
  • Benefits
  • Risks
A
33
Q

For Combined hormonal methods (oral contraceptive pill, ring, patch):

  • MOA
  • Benefits
  • Risks
A
34
Q

For Depot medroxyprogesterone acetate (aka Depo-provera):

  • MOA
  • Benefits
  • Risks
A
35
Q

For Levonorgestrel implant (nexplanon):

  • MOA
  • Benefits
  • Risks
A
36
Q

For Copper IUD (ParaGard):

  • MOA
  • Benefits
  • Risks
A
37
Q

For Levonorgestrel (LNG) intrauterine device (IUD) (mirena, Skyla, kyleena):

  • MOA
  • Benefits
  • Risks
A
38
Q

For Surgical sterilization (vasectomy, tubal ligation, Essure):

  • MOA
  • Benefits
  • Risks
A
39
Q

What are the phases of growth from pre natal to adult and what are the main factors that influence growth at each stage?

A
  • Phases of growth: prenatal → infancy (nutrition) → childhood (growth hormone) → adolescence (growth hormone and sex steroids)
40
Q

What are the maternal factors before and after pregnancy that affect prenatal growth of a baby?

A
  • 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
Q

What are the fetal factors that affect prenatal growth of a baby?

A
  • Fetal factors
    • Familial/chromosomal abnormalities, intrauterine infections (i.e. TORCH – most common infections associated with congenital abnormalities)
42
Q

What are the uterine/placental factors that affect prenatal growth of a baby?

A
  • Uterine/placental factors
    • Inadequate placental growth, uterine malformations, decreased utero-placental blood flow, multiple gestations
43
Q

For intrauterine growth restriction, provide the definition, epidemiology, and co-morbidities (and why this happens)?

A
  • 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
Q

What are the lasting effects of small birth size via IUGR?

A
  • IUGR can lasting effects into adulthood:
    • Small birth size → abnormal glucose/insulin metabolism → increased risk of CVD, diabetes, cognitive disabilities, obesity, and cancers
45
Q

Provide what normal weight gain, normal height gain, and normal growth velocity is?

A
  • 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
Q

How is bone age determined? What bone parts are assessed?

A
  • Bone age: generally use x-ray of left hand → assess epiphysis carpal bones → bone age and predicted adult height
47
Q

When should you be worried about growth?

A
  • Abnormal growth patterns
    • When to worry: height < 3rd percentile, > 97th percentile OR growth velocity < 10th percentile, >95th percentile
48
Q

Provide etiologies of short stature (one big syndrome with sx and tx)?

A
  • 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
Q

Provide etiologies of tall stature divided between childhood and adult

A
  • 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
Q

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
A
51
Q

Define puberty and provide 4 different events in females and males that occur.

A
  • 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
Q

What is the general puberty timing in males and females?

Provide the order of devleopment of different organs.

A
  • 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
Q

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?

A
  • 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
Q

What are pubertal changes associated with estrogen in a female?

Explain the associated tanner changes here.

A
  • 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
Q

What are pubertal changes associated with androgens in a female?

Explain the associated tanner changes here.

A
  • 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
Q

What are pubertal changes associated with testosterone in a male?

Explain the associated tanner changes here.

A
  • 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
Q

Define precocious puberty and the age

A
  • Precocious puberty: early sexual maturation (< 9 y/o for boys, < 8 y/o for girls)
58
Q

How does central precocious puberty work and how is it treated?

A
  • Central: GnRH-dependent sex hormone production → FSH/LH secretion is normal → results in iso-sexual sequential maturation (females → females)
    • Treatment: decide if needed
59
Q

How does peripheral precocious puberty work? Give some etiologies. Give overall tx

A
  • 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
Q

What is McCune Albright syndrome? What signs are associated with it?

What does it cause?

A
  • 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
Q

For benign premature thelarche, provide:

  • description
  • etiology
  • red flags
  • diagnosis
A
  • 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
Q

What are the ages for delayed puberty in each gender?

A
  • Delayed puberty (>13 y/o for girls, >14 y/o for males)
63
Q

What are examples of the following:

  • Constitutional
  • Delayed, but spontaneous
A
  • 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
Q

What are examples of the following:

  • Hypogonadotropic hypogonadism (one syndrome, provide pathophys, sx and tx)
A
  • 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
Q

For hypergonadotropic hypogonadism, provide description, labs, and etiology

A
  • Hypergonadotropic hypogonadism
    • Description: results of gonadal failure, intact HPG axis
    • Labs: elevated FSH
    • Etiology: Turner syndrome, Klinefelter syndrome, irradiation, chemotherapy, infection (dx: karyotype)
66
Q

Provide two examples of unclassified delayed puberty

A
  • 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
Q

Situations for elective and medically induced abortions?

A
  • Elective: unintended pregnancy, domestic issues
  • Medically-indicated: risk to mother’s life, ectopic pregnancy
68
Q

Two meds for medication induced abortion? Provide MOA and SE if any?

When are these indicated?

A
  • 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
Q

Provide surgical methods to abort a baby? Provide MOA and inidcations.

When is a baby viable?

A
  • 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
Q

What are the provider roles in abortion?

A
  • 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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