Exam 2 Flashcards

1
Q

LH in male

A

Leydig cells
Androgen production (DHT, DHEA, testosterone)

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2
Q

FSH in male

A

Sertoli cells
Estrogen production (AMH, inhibin, activin, estradiol)

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3
Q

LH in female

A

Theca cells
Androgen

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4
Q

FSH in female

A

Granulosa cells
Estrogen

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5
Q

Gonadotropin level

A
  • Follicular phase: FSH, LH low
  • Ovulation: LH&raquo_space; FSH
  • Luteal phase: both low
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6
Q

Ovarian cycle

A

tertiary follicle > dominant follicle > ovulation > corpus luteum

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7
Q

Ovarian hormone levels

A
  • Follicular phase: estrogen stimulate the growth of preparation of endometrial cells
  • Ovulation: estrogen > inhibin > progesterone
  • Luteal phase: progesterone prepare endometrium for implantation > inhibin > estrogen
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8
Q

What transports cholesterol into the cell?

A

STAR

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9
Q

What converts cholesterol to pregnenolone?

A

CYP11A1

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10
Q

What is pregnenolone converted into?

A

DHEA or Progesterone

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11
Q

What are DHEA/Progesterone converted into?

A

Androstenedione to testosterone

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12
Q

Which gene encodes aromatase and what does aromatase do?

A

CYP19A1
Convert androgen > estrogen

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13
Q

Steroid hormones are bound to ___ & ___

A

albumin & sex hormone binding globulin (SHBG)

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14
Q

Gonadal peptide hormones types

A
  • Activin A, AB, B
  • Inhibin A, B
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15
Q

Peptide hormones vs steroid hormones mechanism

A
  • Peptide hormones binds to membrane receptor to cross membrane
  • Steroid hormones diffuse across cell membrane
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16
Q

Estrogen receptor alpha predominates in

A

kidney, adrenal, pituitary

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17
Q

Estrogen receptor beta predominates in

A

ovary, lungs, bladder

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18
Q

Estrogen receptor alpha and beta has equivalent expression in

A

mammary gland, uterus, bone, heart, gut, brain

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19
Q

Aromatase deficiency

A
  • Rare
  • Lead to embryonic lethality
  • Two single base pair change in the gene CYP19A1
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20
Q

What levels increase in aromatase deficiency?

A

testosterone and gonadotropin

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21
Q

What levels decrease in aromatase deficiency?

A

androstenedione, estrone, estradiol

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22
Q

Progesterone isoforms

A

PR-A and PR-B

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23
Q

Progesterone receptor present in

A

uterus, breast, uterine tubules, cervix, muscle

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24
Q

Lack of progesterone phenotypes

A

inability to ovulate, uterine hyperplasia and inflammation, limited mammary gland development and an impairment sexual behavior response

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25
Q

What are SERMs

A

Selective Estrogen receptor modulators

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26
Q

Examples of SERMs

A

Tamoxifene, Roloxifene

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27
Q

MOA of Tamoxifene

A
  • antagonist in breast
  • agonist in bone/endometrium
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28
Q

MOA of Roloxifene

A
  • agonist in bone
  • antagonist in breast/endometrium
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29
Q

What are PRMs

A

Progesterone Receptor Modulators

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30
Q

Examples of PRMs

A

Mifepristone, Ulipristone, Asoprisnole

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31
Q

Clinical use of androgen

A
  • replacement therapy- hypogonadism, aging & impotence
  • Protein anabolic/viralizing actions
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32
Q

AEs of androgens

A

fluid retention, edema, congestive HF, kidney failure

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33
Q

What are anti-androgens used to treat?

A
  • prostate cancer
  • hirsutism
  • precocious puberty
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34
Q

Examples of anti-androgens clinical use

A
  • Gonadotropin releasing hormone agonist- continuous feedback inhibition
  • Androgen biosynthesis inhibitor- 5-a-reductase inhibitor
  • Androgen receptor antagonist
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35
Q

What is PCOS?

A

Polycystic Ovary Syndrome

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36
Q

Characteristics of PCOS

A

anovulation, hyperandrogenism, polycystic ovaries

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37
Q

Treatments of PCOS

A
  • Life-style change
  • Combination birth control pill
  • Progestin therapy
  • Clomiphene (ER agonist, induce ovulation)
  • Letrozole (aromatase inhibitor, FSH stimulation)
  • Metformin (improve insulin resistance)
    Gonadotropins (PCOS-induced infertility)
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38
Q

Day 0 of pregnancy (preg)

A

fertilization, fallopian tube

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39
Q

Day 3 of preg

A

Uterus, cell division

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40
Q

Day 6 of preg

A

Implantation in uterus, blastocyst

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41
Q

Day 10 of preg

A

Under the endometrium, embryo

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42
Q

Day 56 to term of preg

A

fetal period

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43
Q

What is fertilization?

A
  • Sperm attaches to outer receptor of the egg
  • Egg becomes nonresponsive to other sperms
  • Membranes combine -> zygote
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44
Q

What is embryonic period?

A

body structure formation

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45
Q

What is fetal period?

A

maturation of structures

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46
Q

G(x)P(TPAL)

A
  • Gravidity- # of preg
  • Parity- # of fetuses delivered after 20 wks of gestation
  • Term deliveries
  • Premature deliveries
  • Aborted/ectopic preg
  • Living children
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47
Q

What is gestational age?

A

Age of the embryo beginning with the first day of the last menstrual period
~2wks prior to fertilization

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48
Q

Calculation of due date

A

Add 7 days to first day of last menstrual period then subtract 3 months

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49
Q

What physiologic markers increase on the mother?

A
  • plasma volume
  • volume of distribution
  • cardiac output
  • weight
  • gastric pH
  • renal, skin, breast BF
  • CYP3A4, 2D6, 2C9
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50
Q

What physiologic markers decrease on the mother?

A
  • albumin
  • BP
  • GI motility
  • CYP1A2, 2C19
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51
Q

Amniotic fluid impact on the fetus

A
  • protects the fetus from injury, infection, provides nutrients and GF
  • allows for fetal movements and breathing
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52
Q

Umbilical cord impact on the fetus

A

exchange of maternal and fetal blood

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53
Q

Placenta impact on the fetus

A
  • composed of maternal and fetal tissue
  • barrier b/w mother and fetus
  • allows for gas exchange, waste removal, and medication transfer
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54
Q

Medication properties to cross placenta

A
  • low MW <600 D
  • lipophilic
  • non-ionized in maternal blood
  • low protein-binding
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55
Q

Non-Medication properties to cross placenta

A
  • fetal-maternal [ ] gradient
  • maternal blood pH less acidic
  • placental BF
  • presence of drug-metabolizing enzymes
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56
Q

What is a teratogen?

A

substance with the potential to alter tissue development or organogenesis

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57
Q

When is the vulnerable time frame for teratogens?

A

week 2 to 8

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58
Q

FDA category
ACE-i and ARBs

A
  • 1st Trimester: C; CV & CNS malformation
  • 2nd&3rd Trimester: D; oligohydraminos, renal failure, patent ductus arteriosus, death
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59
Q

FDA category
Methotrexate

A
  • D/X
  • X in psorias or rheumatoid arthritis
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60
Q

FDA category
Misoprostol

A

X

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61
Q

FDA category
Isotretinoin

A

X

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62
Q

FDA category
Thalidomide

A

X

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63
Q

FDA category
Warfarin

A

X

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64
Q

FDA category
Statins

A

X

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65
Q

FDA category
Paroxetine

A

D

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66
Q

FDA category
Valproic acid

A

D

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67
Q

FDA category
Carbamazepine

A

D

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68
Q

FDA category
Phenytoin

A

D

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69
Q

FDA category
Benzodiazepines

A

D

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70
Q

FDA category
Lithium

A

D

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71
Q

Difference bw DSM-5 vs ACOG criteria

A
  • DSM-5: major depressive episode during preg or in the first 4 wks after delivery
  • ACOG: first 12 months
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72
Q

Pathophys of Major Depressive Disorder (MDD)

A

Unclear, but decreased brain levels of 5-HT, NE, ACh, DA

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73
Q

MDD treatment

A
  1. Psychotherapy = first line in mild-moderate depression
  2. Antidepressants
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74
Q

Antidepressant use in MDD

A

Citalopram, escitalopram, sertraline
- second line in mild-moderate depression
- first line in severe w/ or w/o psychotherapy

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75
Q

Antidepressants with risk

A

Paroxetine, fluoxetine

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76
Q

Antidepressant Discontinuation Syndrome

A
  • Fetus exposed to SSRIs in the third trim
  • resolve w/i 2 to 14 days
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77
Q

Anxiety Disorder treatment

A
  • Psychotherapy preferred in mild or less severe
  • Pharmacological therapy: second-line in mild, first-line in moderate-severe
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78
Q

Pharmacological tx in anxiety disorder: recommended vs not recommended

A
  • Same as depression (citalopram, escitalopram, sertraline)
  • Benzodiazepines not recommended
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79
Q

Why are benzodiazepines not recommended during the first and third trimester?

A
  • First trim: associated w/ cleft lip & palate
  • Third trim: infant sedation and withdrawal symptoms, floppy infant syndrome, hypothermia, lethargy, poor respiratory effort & feeding difficulties
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80
Q

What is iPledge?

A
  • Special rx program for isotretinoin
  • Severe recalcitrant nodular acne
  • Dispense a max quantity for 30 days
  • Pharmacist must obtain PA
  • Require Risk Management Authorization number
  • Med must be dispensed w/i 7 days of preg test
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81
Q

Nonpharmacologic treatment for diabetes

A
  1. Medical Nutrition Therapy (MNT) = primary therapy
  2. Carbohydrate-controlled Meal Plan
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82
Q

When is pharmacological treatment recommended for diabetes?

A

Only when glycemic control cannot be achieved with MNT and exercise

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83
Q

Preferred pharmacological treatment for diabetes

A

Insulin

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84
Q

Insulin lispro
1. onset of action
2. peak of action
3. duration of action
4. preg category

A
  1. 1-15 mins
  2. 1-2 hrs
  3. 4-5 hrs
  4. B
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85
Q

Insulin aspart
1. onset of action
2. peak of action
3. duration of action
4. preg category

A
  1. 1-15 mins
  2. 1-2 hrs
  3. 4-5 hrs
  4. B
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86
Q

Insulin Regular
1. onset of action
2. peak of action
3. duration of action
4. preg category

A
  1. 30-60 mins
  2. 2-4 hrs
  3. 6-8 hrs
  4. B
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87
Q

Insulin NPH
1. onset of action
2. peak of action
3. duration of action
4. preg category

A
  1. 1-3 hrs
  2. 5-7 hrs
  3. 13-18 hrs
  4. B
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88
Q

Metformin use in diabetes

A
  • C/I: lactic acidosis BBW
  • D/c predisposing to hypoxemia
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89
Q

Glyburide/Glipizide use in diabetes

A
  • Glyburide (B/C): d/c at least 2 wks prior to expected delivery date due to risk of hypoglycemia in infant for ~4 days
  • Glipizide (C): d/c at least 1 month prior to the expected delivery date
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90
Q

Nonpharmacological tx for HTN

A
  1. exercise
  2. prevent excessive weight gain
  3. dietary modification: limit sodium intake
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91
Q

Chronic HTN treatment

A
  1. Methyldopa
  2. Thiazide
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92
Q

Preeclampsia-Eclampsia HTN treatment

A
  1. Labetalol

Hydralazine: higher and more frequent associated w/ fetal distress
Nifedipine: reflex tachycardia

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93
Q

Pain relief OTC

A
  1. Acetaminophen
  2. NSAIDs
    - <30 wks gestation (C)
    ->30 wks gestation (D)
    -avoid in 3rd trim

-Aspirin: avoid

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94
Q

Cough and Cold OTC
1. Antihistamine
2. Decongestant

A
  1. Antihistamine choice = Chlorpheniramine
  2. Decongestant choice = Pseudoephedrine (Not first-line for rhinitis)
  • Diphenhydramine: high dose -> oxytocin-like effects
  • Guaifenesin: increased risk of neural tube defects in 1st trim
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95
Q

GI disorder: emesis & diarrhea OTC

A
  1. Kaolin/pectin
  • Bismuth subsalicylate (C, D: >30 wks): not rec due to salicylate absorption
  • Diarrhea w/ infection: X recommend
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96
Q

GI disorder: acid reflux OTC

A
  1. Antacids (Calcium carbonate)
    - Fetal maldevelopment w/ high dose Al, Mg sulfate tocolytic
  2. H2RAs
  3. PPIs
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97
Q

Benefits of breastfeeding: mother

A
  1. decr postpartum bleeding, depression, T2DM, cancer
  2. quicker recovery of pre-preg weight
  3. lactational amenorrhea
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98
Q

Benefits of breastfeeding: infant

A
  1. protective effect against respiratory illnesses, otitis media, GI diseases, allergies
  2. reduced rate of sudden infant death syndrome
  3. reduced adolescent/adult obesity
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99
Q

10 Contraindications to breastfeeding

A
  1. HIV
  2. Untreated brucellosis
  3. HSV w/ breast lesion
  4. Metabolic disorder of classic galactosemia
  5. Human T-cell lymphotrophic virus type I or II
  6. Active TB (can resume after 2 wk tx and no longer infectious)
  7. Varicella
  8. Illicit drug use (narcotic-dependent mothers can breastfeed)
  9. Radioactive exposure, antimetabolite, chemotherapy
  10. Amphetamines, ergotamines, statins
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100
Q

Pain med rec in lac

A
  • NSAIDs- short term use
  • Narcotics- avoid
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101
Q

Immunization C/I in lac

A

small pox, yellow fever

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102
Q

What vaccines are safe during preg?

A
  • Influenza
  • Tdap
  • COVID
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103
Q

What vaccines are NOT safe during preg?

A
  • HPV
  • MMR
  • Varicella
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104
Q

Contraceptive
-Barriers

A

Male/Female condoms, Diaphragm, Cervical Cap, contraceptive sponge, spermicide, withdrawal method, non-hormonal vaginal contraceptive gel

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105
Q

Estrogens risk of thrombotic event directly correlates to ____

A

dose

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106
Q

Progestins are classified based on their ____

A

Estrogenic and androgenic properties

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107
Q

Drospirenone has been found to have ____ properties and is great for ___

A

antiandrogenic, acne

108
Q

Combined Oral Contraceptives (COCs) have same type of A but diff amount of A and B. What’s A and B?

A
  • A = estrogen
  • B = progestin
109
Q

Monophasic COCs

A
  • Same strength of estrogen and progestin
  • Can be used as extended 3-4 month cycle
  • minimize hormone withdrawal and bleeding
  • can be taken continuously w/o placebo wk to avoid menses entirely
110
Q

Multiphasic COCs

A
  • Biphasic: same dose of estrogen w/ two phases of increasing progestin
  • Triphasic: increasing estrogen dose each week (higher risk of BTB)
  • mimics intrinsic estrogen and progestin level the most
111
Q

Extended cycle COCs

A
  • less menstrual periods and symptoms
  • good for heavy menses and dysmenorrhea
112
Q

Progestin-Only Pills (POPs) is recommended for ___

A

Women who are contraindicated with estrogen

113
Q

Disadvantages of POPs

A
  • strict schedule: at the same time
  • frequent BTB
  • increased risk of ectopic pregnancy
114
Q

Time scheduling of POP & how many hours late is considered missed dose?

A
  • Strict, same time
  • 3 hrs late = missed dose
115
Q

Use of POPs show less efficacy in ___

A

pts >70 kg

116
Q

When do you use back up contraceptives for 7 days with patches?

A
  1. patch off or partially off for >24 hrs
  2. patch not changed/restarted for 9 days
117
Q

What do you if you miss patch in 3rd week?

A

Omit placebo patch

118
Q

Using patches results in decreased efficacy in patients _____

A

> 90 kg, BMI > 30 kg/m^2

119
Q

What do you do if NuvaRing gets removed accidently?

A
  • <3hrs: rinse with water and reinsert
  • > = 3 hrs: above + back up method for 7 days
120
Q

What do you do if Annovera gets removed accidently?

A
  • <2hrs: wash with soap and water, rinse and pat dry, and reinsert
  • > =2 hrs: back-up contraception for 7 days
121
Q

Advantage of DMPA

A
  • no alteration in BP
  • no increase risk of VTE
  • reduce risk of endometrial cancer
  • can treat endometriosis
  • less drug-drug interaction
122
Q

Disadvantage of Depo Medroxyprogesterone Acetate (DMPA)

A

BBW, menstrual irregularities, weight gain, decrease glucose intolerance

123
Q

BBW of DMPA

A
  • Short term bone loss in younger women of reproductive age
  • Should not use long term >2 yrs
124
Q

SEs of LNG-IUD

A
  • increased BTB and spotting with first 3 to 6 months
  • may see absence of menses after 1 yr
  • infections
125
Q

LNG-IUD needs seeking immediate medical care with PAINS. What is PAINS?

A
  • Period is late
  • Abdominal pain
  • Infection
  • Not feeling well
  • String is missing/shorter/longer
126
Q

Copper-releasing IUD is approved for use of how long?

A

10 years (long lasting)

127
Q

How long etonogestrel-releasing implant good for?

128
Q

How is etonogestrel-releasing implant inserted?

A

Subdermally in upper arm by certified provider

129
Q

When converting from oral COCs to Etonogestrel-releasing implant, insert ____

A

within 7 days of last active pill

130
Q

When converting from patch/ring/IUD to etonogestrel-releasing implant, insert ____

A

on day of removal of patch/ring/IUD

131
Q

D/I contraceptives counseling point: moderate/potent CYP inducers may _____ of oral contraceptives and need ____ of estrogen

A

decrease the efficacy, increase doses

132
Q

D/I contraceptives counseling point: back-up methods are recommended for at least 2 weeks after completion of therapy of:

A

rifampin, anticonvulsants (phenytoin, carbamazepine), steroid, St. John’s Wort

133
Q

When the pt missed 1 pill COC

A
  • take late or missed pill ASAP
  • continue with regular schedule
  • taking two pills on same day if needed
134
Q

When the pt missed >=2 consecutive pills COC

A
  • take MOST RECENTLY missed pill ASAP
  • discard remaining missed pills
135
Q

When pt missed pills during the 3rd week COC

A
  • omit hormone-free interval
  • start new pack immediately
  • if unable, use back-up methods until pills are taken for 7 consecutive days of new pack
136
Q

Missed dose for POPs

A
  1. dose is considered missed if >3 hrs late
  2. take one pill ASAP
  3. use non-hormonal methods until pills are taken correctly for 2 consecutive days
137
Q

Key counseling points for COCs AEs: ACHES

A
  • Abdominal pain
  • Chest pain
  • Headaches
  • Eye problem
  • Severe leg pain or swelling
138
Q

Emergency contraception in order of efficacy: levonorgestrel, ulipristal, Copper IUD, Yuzpe

A

Copper IUD > ulipristal > levonorgestrel > Yuzpe

139
Q

Copper IUD insertion: at where and within how many days of intercourse?

A

at doctor’s office, within 5 days

140
Q

Copper IUD preferred in ____

141
Q

When do you take Ulipristal acetate?

A

ASAP within 120 hrs

142
Q

Ulipristal decreased efficacy in pts with BMI ____

A

> 25 kg/m2

143
Q

Levonorgestrel (progestin) dosage and initiation within how many hrs?

A
  • Single or two-dose regimen within 72 hrs of intercourse
  • 1.5mg ASAP or 0.75mg ASAP + 0.75mg 12 hrs after the first dose
144
Q

Levonorgestrel decreased efficacy in pts with BMI _____

A

> 25 kg/m2

145
Q

How do you take Yuzpe regimen

A

2T PO Q 12 H

146
Q

When should antiemetic should be given with Yuzpe?

A

1 to 2 hrs prior to each dose

147
Q

Emergency contraceptives key counseling points

A
  1. directions for use and SE
  2. EC is NOT for routine contraception
  3. does NOT protect against STIs
  4. if on hormonal contraceptives, can continue with regular scheduled dose
  5. pregnancy test if normal period does not return within 3 wks of therapy
148
Q

Symptoms of menopause

A
  • Sleep disturbances
  • Genitourinary (GU) syndrome
  • Cognitive changes
  • Hot flashes
149
Q

Hot flashes treatment challenge

A

duration of tx limited to 4 to 5 yrs to avoid excess breast cancer risk

150
Q

Recommended non-pharmacological therapy for menopause

A
  • Weight loss
  • Cognitive-Behavioral therapy
  • Clinical hypnosis
151
Q

Consideration criteria for hormone therapy in menopause

A
  1. menopausal women <60
  2. within 10 yrs of final menstrual period
  3. without C/I
152
Q

Greater risk w/ hormone therapy in menopause

A

women >60 yrs or >10 yrs beyond menopause onset

153
Q

Highest risk w/ hormone therapy in menopause

154
Q

Women with an intact uterus using systemic estrogen therapy should receive adequate ______, unless taking CEE + ______

A

progestogen, bazedoxifene

155
Q

Non-hormonal therapy SSRI in menopause

A

escitalopram, citalopram, paroxetine

156
Q

Non-hormonal therapy SNRI in menopause

A

Venlafaxine, desvenlafaxine

157
Q

Other Non-hormonal therapy in menopause

A

oxybutynin, gabapentin

158
Q

Non-hormone therapy for vaginal symptoms in menopause

A

Ospemifene

159
Q

Ospemifene BBW

A

endometrial cancer, stroke, VTE

160
Q

Ospemifene can be used for long-term treatment in menopause vaginal atrophy: T/F

A

F
- use shortest duration due to BBW

161
Q

Not recommended non-hormonal therapy in menopause

A

pregabalin, clonidine, suvorexant

162
Q

Extended use of hormonal therapy in menopause for >65 yo

A

-Reasonable in healthy individuals with persistent VMS >65
- need counseling, regular risk assessment, shared decision making

163
Q

Discontinuing hormone therapy in menopause

A
  • symptoms recur 50%
  • taper > abrupt d/c
  • long-term low dose vaginal estrogen therapy safe
164
Q

All estrogen products used for menopause carry BBW:
BCDE

A
  • Breast cancer
  • Cardiovascular disease (stroke, MI, VTE)
  • Dementia: >=65 yrs
  • Endometrial cancer: when estrogen used alone
165
Q

What is infertility?

A

Failure to achieve clinical pregnancy after 12 months or more of regular unprotected sexual intercourse if <35 yrs old

  • 6 months if >= 35 yrs
166
Q

Contributing factors of infertility

A
  1. Age: decline by age 30
  2. Hx of pelvic infections or STD
  3. Tobacco, alcohol, illicit drug use
  4. Weight extremes
  5. Excess exercise
167
Q

Primary causes of infertility

A

3:3:2:2 = female:male:mixed causes:UKN

  • female:male = 1:1
168
Q

Diagnosis of PCOS

A
  • irregular periods
  • hyperandrogenism
  • polycystic ovaries
169
Q

First line treatment of PCOS

A

Clomiphene

170
Q

Days 1-4: FSH level ____

171
Q

Days 5-7: FSH level ____, estradiol ____ in response to ______

A

decrease, increase, low FSH

172
Q

Days 13-14: LH level ____, FSH level ___

A

increase (LH surge), small increase spike

173
Q

Peak fertility is on days _____

174
Q

Egg is fertile for ____ hrs

175
Q

Sperm survives ___ hrs

176
Q

During luteal phase, progesterone level ____ and estradiol level ____, produced by ____ results in _____

A

increase, increase, corpus luteum, optimizing conditions for oocyte

177
Q

What happens if the egg is NOT fertilized during the luteal phase?

A
  • drop in hormones
  • endometrial tissue breaks down
178
Q

Clomiphene is first line treatment for ___, ___, or ___.

A

anovulation, PCOS, unexplained infertility

179
Q

Clomiphene MOA

A

interferes with (-) feedback of estradiol produced by follicles that normally suppress FSH/LH release –> stimulate release of FSH & LH

180
Q

Clomiphene dose for healthy vs PCOS

A

healthy: 50 mg QD x5days
PCOS: 25 mg/day

181
Q

2 hormones released from thyroid gland

A
  • Thyroid hormones (T3, T4)
  • Calcitonin
182
Q

How are thyroid hormones stored?

A

Stored as amino acid residues in thyroglobulin which constitutes majority of thyroid follicular colloid

183
Q

Thyroid hormone synthesis steps

A
  1. Uptake of iodide (iodide trapping)
  2. Iodide organification (oxidation, iodination)
  3. Coupling of MIT and DIT
  4. Secretion of thyroid hormones
  5. Conversion of T4 to T3 (deiodination)
184
Q

Thyroid hormones are derivatives of _____.

A
  • tyrosine
  • ONLY L-isomers are active
185
Q

What stimulates iodide trapping and what inhibits it?

A
  • uptake process: from blood -> thyroid follicular cell via Na+/I- symporter
  • autoregulatory system: low iodide storage = increased uptake
  • stimulated by: TSH (from AP)
  • inhibited by monovalent anions: perchlorate, pertechnetate, thiocyanate (PPT)
186
Q

What is thyroid peroxidase and what drug inhibits this?

A
  • heme containing enzyme that uses hydrogen peroxide derived from oxidizing NADPH in order to oxidize iodide to iodine (during organification)
  • also oxidizes the coupling reaction of MIT and DIT to form T3 and T4
  • inhibited by thionamides
187
Q

How are T3 and T4 released?

A

Proteolysis of T3 & T4 stored w/in TG
1. endocytosis of TG/colloid from follicular lumen
2. fusion w/ lysosomal granules containing proteolytic enzymes
3. TG breakdown -> secretion of T3 & T4

188
Q

T4 vs T3 which is more potent?

189
Q

How are T3 and T4 protected against metabolism?

A

they reversibly bind to thyroxine binding globulin (TBG) and transthyretin

190
Q

Deiodination of T4 to T3 is mediated by ____

A

5’-deiodinase

191
Q

What inhibits the iodide uptake?

A
  • Bromine Fluorine Lithium
  • Thiocyanate Perchlorate Pertechnetate
192
Q

What inhibits T3 and T4 secretion?

A
  • Iodide (large dose), Lithium
193
Q

What inhibits organification and coupling?

A
  • thionamides, sulfonylurea, sulfonylamides, salicylamide
194
Q

Cytoplasmic receptors bind ____

195
Q

Membrane receptors (αVβ3 integrin) bind ____

196
Q

What is Cretinism?

A

Lacking iodine –> failure of thyroid to develop during infancy –> dwarfism, mental retardation, pale skin, slow heart rate, low body temp

197
Q

Direct vs indirect effect of thyroid hormone on heart & what is the end result?

A
  • Direct: Binds to thyroid hormone receptor in heart
  • Indirect: increased number of beta receptor in heart
  • Result: increased hr, force of contract –> increased CO
198
Q

AIT-I vs AIT-II

A

AIT-I is associated with increase in iodine load and most likely to occur in patients with pre-existing thyroid disease

AIT-II is destructive thyroiditis and causes the release of preformed hormone from damaged thyroid gland

199
Q

Trend of thyroid test in hyperthyroidism vs hypothyroidism

A
  • Hyperthyroidism: decrease in TSH, increase in total T4 + T3, free T4, and T3 resin uptake
  • Hypothyroidism: increase in TSH, decrease in total T4 + T3, free T4, and T3 resin uptake
200
Q

Drugs that increase TH secretion

A

iodide, amiodarone (AI)

201
Q

Drugs that decrease TH secretion

A

iodide, amiodarone, lithium (LIA)

202
Q

Ab, RAIU lab results & S/S of Graves Disease

A
  • TSAb present
  • RAIU elevated
  • Exophthalmos, pretibial myxedema, acropachy
  • Enlarged thyroid (x2-3 normal size)
  • Systolic bruit heard over thyroid gland via stethoscope
203
Q

Pros and cons of surgery to treat hyperthyroidism

A
  • Pros: rapid, effective, :) in pregnancy
  • Cons: most invasive, potential nerve damage, costly, hypothyroidism
204
Q

Pros and cons of radioactive iodine to treat hyperthyroidism

A
  • Pros: most effective, cure, best treatment for toxic nodules
  • Cons: hypothyroidism, pregnancy must be deferred 6-12 mo
205
Q

Pros and cons of anti-thyroid medication to treat hyperthyroidism

A
  • Pros: non-invasive, low cost, low risk of hypothyroidism, initial therapy in severe cases or pre-operation
  • Cons: low cure rate, side effects
206
Q

Candidates for hyperthyroidism surgery

A
  1. Patients with thyroid glands >80g
  2. Severe ophthalmopathy (vision problem)
  3. Failure with antithyroid medications
207
Q

Thioureas as hyperthyroidism tx: MoA, examples

A
  • MoA: inhibition of organification of iodine into thyroglobulin and coupling
  • Examples:
    1. PTU (propylthiouracil) : preferred in 1st trim preg
    2. MMI (methimazole) : preferred except for pregnancy
208
Q

Keys to success in using thiourea to treat hyperthyroidism

A
  • Older than 40
  • Low T4:T3 < 20 (high T4, low T3)
  • Small goiter <50
  • Short duration 6 mo within diagnosis
  • Length of therapy 1-2 yrs or longer
  • Low TSAb titers
209
Q

AEs of thioureas as hyperthyroidism tx

A
  • PTU: Hepatotoxicity, MMI: Acute pancreatitis
  • Pruritic maculopapular rash, fevers, arthralgias, benign transient leukopenia, agranulocytosis (ANC < 250 d/c), GI distress
210
Q

AEs of iodides in hyperthyroidism tx

A
  • Hypersensitivity reactions
  • Salivary gland swelling (b/c it is given PO)
  • Iodism (metallic taste, burning mouth, sore teeth/gum, GI upset, head cold, gynecomastia)
211
Q

When should iodides therapy be initiated regarding pre-op and after RAI to treat hyperthyroidism?

A

7-14 days before surgery or 3-7 days after RAI therapy

212
Q

Hyperthyroidism Beta Adrenergic Agents: MoA and Example

A

Only as adjunctive therapy
- MoA: block the adrenergic related symptoms of hyperthyroidism such as palpitations, anxiety, tremor, heat intolerance
- Examples:
1. Propranolol
2. Diltiazem if C/I

213
Q

RAI (iodine 131) is first line option in hyperthyroidism for ____

A
  1. Grave’s disease
  2. Toxic autonomous nodules
  3. Multinodular goiter
214
Q

Types of primary hypothyroidism

A
  • Hashimoto’s disease
  • Iatrogenic hypothyroidism (after RAI therapy or surgery)
  • Iodine deficiency, thyroid hypoplasia, medications
215
Q

S&S of Hashimoto’s Disease

A

Thyroid gland enlargment or thyroid gland atrophy –> cannot be diagnosed w/o testing if antithyroid peroxidase antibodies are present

216
Q

Iodine deficiency is the most common cause of ___

A

preventable mental deficiency

217
Q

Drug of choice for hypothyroidism

A

Levothyroxine

218
Q

Replacement dosage and maintenance dosage of levothyroxine

A
  • 1.7mcg/kg/day
  • 125mcg
219
Q

Initial dose of levothyroxine for elderly or cardiac disease pts vs healthy pts

A
  • 12.5-25 mcg/day
  • 50-100 mcg/day
220
Q

Dosage adjustment for a hypothyroid patient on levothyroxine who finds out she is pregnant

A

increase dose by 20-30%

221
Q

What are drugs that are affected by hyper/hypothyroidism (in terms of their PK)

A

digoxin, warfarin

222
Q

Levothyroxine pt counseling

A
  • Maximal absorption takes about 2 hours
  • Food can impair absorption, so dosing in regards to food should remain consistent -> empty stomach!
  • Cholestyramine, ferrous sulfate, sucralfate, Ca supplements, antacids, dietary fiber, coffee, PPIs, histamine blockers will decrease absorption
223
Q

Myxedema coma: def & treatment

A
  • Long-standing hypothyroidism that is untreated
  • IV levothyroixine, hydrocortisone
224
Q

Subclinical hypothyroidism: def & treatment

A
  • Asymptomatic patients with altered thyroid function tests (elevated TSH, normal T3, T4)
  • Treating this patient is controversial - maybe start levothyroxine 25-50mcg daily and monitor TSH
  • Treat if TSH > 10 v.s. Monitor if TSH < 10
225
Q

Progestin risk of thrombosis correlates with ____

A

generation

226
Q

RAI as hyperthyroidism tx is contraindicated in

227
Q

SE of RAI hyperthyroidism tx

A

Long term toxicity may lead to hypothyroidism

228
Q

Absolute C/I for estrogen-progestin contraceptives

A
  1. > =35 yrs + >=15 cigarettes/day
  2. <21 days postpartum
  3. Breast/genital tract cancer
  4. Hx or current VTE and/or stroke
  5. Multiple CAD risk factors
  6. Ischemic heart disease
  7. SBP >=160, DBP >=100
  8. Liver disease
  9. Migraines with aura
229
Q

Which non-hormonal barrier contraceptives require concomitant use of spermicide: cervical cap or contraceptive sponge?

A

Cervical cap

230
Q

Natural method contraceptive: Basal Body Temperature; BBT drops ___ to ___ hrs before ovulation and then increases by __ to __ •F above the lowest point over __ to __ hr period

A
  • 12 to 24 hrs
  • 0.4 to 0.8 •F
  • 24 to 48 hr period
231
Q

Avoid using contraceptive sponge when:

A
  1. Menstrual period
  2. Within 6 wks of childbirth
  3. Sulfite allergy
  4. Hx of toxic shock syndrome
232
Q

When no hormonal contraceptive is used within the past month, insert etonogestrel-releasing implant on days __ to __ of menstrual cycle

A

1 to 5 days

233
Q

DMPA takes average of ___ to return to fertility while etonogestrel-releasing implant takes ___

A

10 months vs 30 days

234
Q

Contraceptive SE mood change is more common with ____

235
Q

Contraceptive SE weight gain is due to ___. This effect can be combatted with ___.

A
  • Estrogen causing water retention -> weight gain
  • Drospirenone
236
Q

Low dose estrogen is used for contraceptives in pts who are ___

A
  • healthy
  • > =35 yrs
  • adolescents
  • underweight <50 kg
  • no DDI
237
Q

Medium dose estrogen is used for contraceptives in pts who are ___

A
  • non-adherence
  • overweight
238
Q

High dose estrogen is used for contraceptives in pts who are ___

A
  • Heavy menses
  • DDI
  • failure with lower doses
239
Q

Progestin only is used for contraceptives in pts who are ___

A
  • > =35 yrs + smoking
  • breastfeeding / lactating
  • CVD
  • estrogen dependent cancer
  • postpartum
  • hx of VTE
  • migraines
240
Q

What is gender/gender identity?

A

A person’s internal sense of self and how they fit into the world, from the perspective of gender

241
Q

What is sex?

A

Sex assigned at birth

242
Q

What is gender expression?

A

The outward manner in which an individual expresses or displays their gender

243
Q

What is transgender?

A

A person whose gender identity differs from the sex that was assigned at birth

244
Q

What is cisgender?

A

A person whose gender identity is the same from the sex that was assigned at birth

245
Q

What is gender dysphoria in adults?

A

Lasting at least 6mons w/ at least 2 of the following symptoms:
- Marked incongruence bw one’s experienced/expressed gender and primary sex characteristics
- strong desire to be rid of one’s primary and/or secondary sex characters
- strong desire to be of the other gender
- strong desire to be treated as the other gender
- strong conviction that one has the typical feelings and rxns of the other gender

246
Q

General tx rec for gender affirming care

A
  1. Psychological assessment
  2. Hormone tx
  3. Genital surgery
247
Q

First line therapy for male to female transition:

A
  1. Estrogen
  2. Estrogen + Spironolactone (Androgen blocker)
248
Q

What estrogen therapy would you recommend to pts with history or risk of VTE for male to female transition?

A

Estradiol transdermal patch

249
Q

What are second line androgen blockers used for male to female transition?

A

Finasteride, Dutasteride

250
Q

What can be added as supplemental therapy in addition to the first-line tx for male to female transition?

A

Progestogen

251
Q

What lab should be monitored only if spironolactone is used in male to female transition?

252
Q

What is the general hormone therapy for female to male transition?

A

Testosterone

253
Q

What is an absolute contraindication to testosterone tx in female to male transition?

A

Hx of breast cancer

254
Q

What testosterone tx is not the first-line tx in female to male transition?

A

Testosterone undecanoate

255
Q

Comorbidities in transgender health

A
  1. CVD
  2. DM
  3. Bone health & osteoporosis
  4. HIV
  5. Hepatitis C
  6. STIs
256
Q

CVD in transgender health

A

Females:
- Predicted increased risk
- Estrogen: use transdermal patch > oral
Males:
- No change in risk

257
Q

DM in transgender health

A
  • Screening rec do not differ from current national guidelines for general pt populations
  • Decreasing risk factors prior to hormone tx
  • No clear rec
  • Adequate control A1c <7
258
Q

Known risk factors of Bone health & Osteoporosis in transgender health:

A
  1. Caucasian or Asian
  2. Older age
  3. Alcohol >10 drinks/wk
  4. Low BMI
  5. Smoking
  6. Chronic corticosteroid use
  7. Hypogonadism
  8. Rheumatoid arthritis
  9. Hyperparathyroidism
  10. Immobility
  11. Vit D deficiency
  12. HIV infection
259
Q

Bone health & Osteoporosis in transgender health:

A

Transgender women:
- Levels of physical activity, muscle mass and grip strength, lower levels of Vit D
- After hormones: lower/higher/no change in Bone Mineral Density (BMD)
Transgender men:
- No change or increase in BMD

260
Q

What is the current screening of Bone health & Osteoporosis in transgender health?

A
  • No consistency
  • WHO every 10 yrs
  • Varying yrs in changes in bone density
  • All non-transgender women >65 yrs
261
Q

What is the recommended screening of Bone health & Osteoporosis in transgender health?

A
  • Should begin at age 65
  • Ages 50 and 64 -> increased risk for osteoporosis
  • Those who have undergone gonadectomy w/ hx of 5 yrs w/o hormonal replacement should be considered for testing
262
Q

HIV in transgender health

A
  • Services should address: biological, psychological, social needs
  • Experiences: high rates of trauma, unstable housing, poverty, incarceration, unemployment
  • Anatomy-specific sexual behavior
  • Prevention: condoms, PrEP, nPEP
  • HIV tx: DDI’s
263
Q

Hepatitis C in transgender health:

A
  • Needlestick exposure
  • Monitor liver function
  • Non-oral hormone tx
  • DDIs
264
Q

Sexually Transmitted Infections in transgender health:

A
  • Screen every 3 months for high-risk individuals
  • May avoid screening
  • Sexual hx and risk assessment
  • Physical exam & STI screening
265
Q

Role of a pharmacist in gender affirming care

A
  1. Discussing specific hormone tx
  2. Monitoring lab values
  3. Identifying risk reduction strategies
  4. Reduce barriers to care
  5. Implementation of systemic changes w/i the system