Pharm Flashcards

1
Q

Warfarin is in what pregnancy category?

A

Category X

worst, completely contraindicated

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2
Q

Surfactant deficit in immature lungs often leads to:

A

Respiratory distress syndrome (RDS)

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3
Q

RDS affects 40-50% of babies born before what week of pregnancy?

A

Week 32

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4
Q

Endogenous fetal cortisol drives lung maturation. Therefore administration of what “fills” the fetal cortisol deficit at weeks 24-34?

A

Betamethasone

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5
Q

Glucocorticoid (betamethasone) administration promotes the transcription of:

A

Surfactant proteins

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6
Q

Surfactant proteins affect which cells in lung?

A

Type II pneumocytes

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7
Q

Why can’t we just administer cortisol antenatally?

A

The placenta inactivates cortisol because it is rich in 11ß-hydroxy steroid dehydrogenase-2 (11ß-HSD-2)

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8
Q

Commonly used drug to delay labor:

A

MgSO4

  • used for 24-48 hour delays
  • allows time for a concurrent course of corticosteroids to act in a pre-term birth (24-32 weeks)
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9
Q

Tocolytic drugs:
Ritodrine
Salbutamol
Terbutaline

MOA?

A

B2 agonists -> relaxes uterine SM

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10
Q

Tocolytic drug:
Indomethacin (NSAIDs)

MOA?

A

Inhibits uterine COX-1 enzyme ->

Blocks PGF2a and PGE2 formation

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11
Q

Tocolytic drug:
Nifedipine

MOA?

A

Ca2+ channel antagonist (voltage-gated L channels) -> relaxes uterine SM

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12
Q

Tocolytic drug:
MgSO4

MOA?

A

Competition at Ca2+ channels

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13
Q

Tocolytic drug:
Atosiban

MOA?

A

Oxytocin pituitary neuropeptide receptor antagonist (only in Europe)

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14
Q
TQ
AEs of B2 agonists:
-Ritodrine
-Salbutamol
-Terbutaline
A

Tachycardia
Hypotension
Hypokalemia*
Hyperglycemia*

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15
Q

TQ

AEs of using indomethacin at term: (2)

A

Closure of the ductus arteriosus in utero (fetus)
-only given in 2nd trimester

Bleeding risk, ulcer (mother)

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16
Q

AEs of nifedipine: (2)

A

Dizziness and hypotension in the mother

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17
Q

MgSO4 is contraindicated in:

A

Myasthenia gravis

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18
Q

MOA of oxytocin:

A

Induces oxytocin receptors on uterus to promote uterine contraction

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19
Q

Favored drug for inducing labor:

A

Oxytocin

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20
Q

Test for fetal viability:

A

Oxytocin challenge test

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21
Q

TQ

What pharmaceutical agent is used to ripen the cervix?

A

Dinoprostone (PGE2)

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22
Q

TQ

In utero, COX-1 and COX-2 both make ____, which binds to __ receptors in the ductus arteriosus.

A

In utero, COX-1 and COX-2 both make PGE2, which binds to EP receptors in the ductus arteriosus.

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23
Q

What happens to PGE2 at birth?

A

Maturation of the neonatal lung metabolizes PGE2 and withdraws its effects on the ductus arteriosus – ductus arteriosus closes.

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24
Q

TQ

Drug to maintain a ductus arteriosus: in congenital heart disorders:

A

PGE1 (Alprostadil)

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25
Q

TQ

What is molecular target of dinoprostone (PGE2) and alprostadil (PGE1)?

A

EP

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26
Q

Molecular target of PGI2 (prostacyclin):

A

IP

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27
Q

Molecular target of PGF2a:

A

FP

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28
Q

Molecular target of TxA2:

A

TP

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29
Q

TQ

Complications of PGE1 (Alprostadil) administration:

A

Hypotension
Tachycardia
Apnea
Pyrexia (fever, raised body temp) ***

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30
Q

TQ

Drug to close PDA in *premature:

A

Indomethacin (NSAIDs)

“ENDomethacin”

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31
Q

NSAIDs inhibits COX1 and COX2 ->
Deficit of PGE, PGI ->
Renal vasoconstriction -> (4)?

A

Na+ and H2O retention (oliguria, edema)
Reduced Cr clearance (high serum Cr)
Mild HTN

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32
Q

TQ

Sulfonamide use can cause what pediatric catastrophe?

A

Kernicterus

-Neonatal encephalopathy due to bilirubin displacement and poor bilirubin clearance

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33
Q

TQ
Neonate presents with abdom distension, diarrhea, vomiting, dusky gray color, circulatory collapse and death.

What drug was given?

A

Chloramphenicol

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34
Q

TQ

Gray baby syndrome is due to:

A

Impaired glucuronidation in neonates

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35
Q

TQ
Tetracycline(s) are pregnancy category D.
What do tetracyclines cause?

A

Fatty liver hepatotoxicity

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36
Q

AE of fluoroquinolones:

A

Cartilage erosion

Do not administer age < 18

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37
Q

AE of tetracyclines:

A

Bone, teeth deposits

(Do not administer

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38
Q

Aspirin given to a child with a viral illness will cause:

A

Reye’s syndrome

Hospitalization to stop brain and liver damage

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39
Q

First line Rx for chlamydia:

A

Azithromycin (+ doxycycline)

Use amoxicillin during pregnancy.

40
Q

First line Rx for gonorrhea:

A

Ceftriaxone

41
Q

First line Rx for 1º (2º, early latent) syphilis:

A

IM Benzathine penicillin G

42
Q

Rx for vulvovaginal candidiasis:

A

Fluconazole (single dose)

Miconazole (vaginal application, topical)

43
Q

Rx for trichomonas vaginalis:

A

Metronidazole

44
Q

Rx for bacterial vaginosis (Gardnerella, Mycoplasma…):

A

Metronidazole

Clindamycin (vaginal cream)

45
Q

Rx for pubic lice, crabs, scabies: (2)

A

Permethrin

Ivermectin

46
Q

Rx for genital herpes: (3)

A

Acyclovir
Famciclovir
Valacyclovir

47
Q

Bed sores or pressure ulcers in an HIV pt that are difficult to heal. Think…

A

Herpes

48
Q

PAINLESS ulcers at inoculation site:
Rash and adenopathy:
Cardiac, neurologic, ophthalmologic and gummatous manifestations:

A

PAINLESS ulcers at inoculation site with clear base: 1º syphilis
Rash (hands and feet) and adenopathy, condyloma lata: 2º syphilis
Cardiac, neurologic, ophthalmologic and gummatous manifestations: 3º syphilis

49
Q

Men: Urethritis
Women: dysuria, thin vaginal discharge, post-coital bleeding***, may present with PID

A

Chlamydia

50
Q

Men: dysuria and discharge appear within 2-5 days (95% symptomatic)

Women: dysuria, thick, yellow discharge, vaginal bleeding, vaginal pain
-May present with PID

A

Gonorrhea

51
Q

Extra-genital manifestations of gonorrhea: (5)

A
Septic arthritis*
Purpuric skin lesions
Pharyngitis
Endocarditis
Fitz-Hugh-Curtis syndrome
52
Q
  • Malodorous, frothy yellow/green discharge
  • “Strawberry cervix”
  • Flagellated organisms on wet prep
A

Trichomonas

53
Q

Primary goal for tx of visible HPV warts is:

A

Removal of symptomatic warts

54
Q

HPV vaccine is activate against which serotypes?

A

16 and 18

55
Q

Recommended regimens of Pediculosis pubis (on pubic hair):

A

Permethrin 1%***
Lindane 1% shampoo
Pyrethrins with piperonyl butoxide

56
Q

Pharmacologic effects of HCs: (5)

A
  • Modify mid‐cycle surges of luteinizing hormone (LH) & follicle‐stimulating hormone (FSH)
  • Inhibit ovulation by suppressing function of the hypothalamic‐pituitary‐ovarian axis
  • Diminish ovarian hormone production
  • Produce endometrial changes unfavorable for ovum implantation
  • Thicken cervical mucus to impede sperm transit
57
Q

Estrogens in oral HCs: (3)

A
  • Ethinyl estradiol (EE) (most common entity in HCs)
  • Estradiol valerate (pro-drug)
  • Mestranol
58
Q

What drug is the only non-hormonal preparation with progestin-like activity?

A

Drospirenone

spironolactone analog

59
Q

Which drug is considered to best drug of start HC therapy due to equal levels of progestin, estrogen, and androgens?

A

Norethindrone

60
Q

Receptor effects of desogestrel:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of desogestrel:

  • Progestinic: ++++
  • Estrogenic: 0
  • Androgenic: +++
61
Q

Receptor effects of levonorgestrel:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of levonorgestrel:

  • Progestinic: ++++
  • Estrogenic: 0
  • Androgenic: ++++
62
Q

Receptor effects of norgestrel:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of norgestrel:

  • Progestinic: +++
  • Estrogenic: 0
  • Androgenic: +++
63
Q

Receptor effects of ethynodiol diacetate:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of ethynodiol diacetate:

  • Progestinic: ++
  • Estrogenic: +++
  • Androgenic: +
64
Q

Receptor effects of norgestimate:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of norgestimate:

  • Progestinic: ++
  • Estrogenic: 0
  • Androgenic: ++
65
Q

Receptor effects of norethindrone (and norethindrone acetate):

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of norethindrone (and norethindrone acetate):

  • Progestinic: ++
  • Estrogenic: ++
  • Androgenic: ++
66
Q

Receptor effects of drospirenone:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of drospirenone:

  • Progestinic: ++
  • Estrogenic: 0
  • Androgenic: 0
67
Q

Receptor effects of dienogest:

  • Progestinic:
  • Estrogenic:
  • Androgenic:
A

Receptor effects of dienogest:

  • Progestinic: ++
  • Estrogenic: 0
  • Androgenic: 0
68
Q
  • Non-oral progestin
  • Metabolite of norgestimate
  • Available in a patch with EE (7 days)
A

Norelgestromin

do NOT take if not supposed to take estrogens…

69
Q
  • Non-oral progestin
  • Metabolite of desogestrel
  • Available in vaginal ring with EE (3 weeks)
  • Available in progestin-only implantable rods (3 years)
A

Etonogestrel

70
Q
  • Non-oral progestin

- Available in progestin-only, long-acting injection (3 months)

A

Medroxyprogesterone

71
Q

-Non-oral progestin
-Available in progestin-only intrauterine device (IUD)
(Mirena = 5 years)
(Skyla = 3 years)

A

Levonorgestrel

72
Q

Common HC adverse effects: (6)

A
  • Irregular bleeding
  • Breast tenderness
  • Fluid retention (weight gain)
  • Mood changes
  • Headaches and GI distress
  • Hyperkalemia (drospirenone)*
73
Q

Serious adverse effects of HCs: (3)

A
  • Systemic thromboembolism (MI / stroke / DVT / PE/intestinal ischemia)
  • HTN
  • Gallbladder dz
74
Q

TQ

HC contraindications: (6)

A
  • Hx of vascular-related dz’s
  • Known or suspected pregnancy
  • Breast / endometrial / hepatic neoplasms
  • Undiagnosed vaginal bleeding
  • Uncontrolled HTN
  • **Smoking in pts ≥35yo **
75
Q

TQ
2-dose drug used for emergency contraception:
What is its MOA?
Within how many hours must the pt take the first dose?

A

Levonorgestrel

  • MOA: Inhibition of ovulation
  • 1st dose within 72 hours* (2nd dose 12 hours after)
76
Q

TQ
1-dose (non-progestin) drug use for emergency contraception:
What is its MOA?
Within how many hours must the pt take the first and only dose?

A

ella (ulipristal)

  • Progesterone receptor modulator – main action is inhibition of ovulation
  • Dose within 120 hours
77
Q

TQ
The primary therapy for menopause is estrogen.
Women with an intact uterus must also be on a _________.

A

The primary therapy for menopause is estrogen.
Women with an intact uterus must also be on a PROGESTIN.

(i.e., if she underwent a hysterectomy, no need for progestin in regimen)

78
Q

Menopausal hormone therapy

Available estrogen Rx’s: (6)

A
  • Estradiol
  • Conjugated estrogens (equine; CEE) – “natural” hormone
  • Synthetic conjugated estrogens-A
  • Synthetic conjugated estrogen-B
  • Esterified estrogens (EE)
  • Estropipate (generic, stabilized with piperazine)
79
Q

Menopausal hormone therapy

Available progestinic Rx’s: (7)

A
  • Medroxyprogesterone (MPA)
  • Methyltestosterone
  • Progesterone
  • Norgestimate
  • Norethindrone/Norethindrone acetate
  • Drospirenone
  • Levonorgestrel
80
Q
TQ
Estrogen-only hormone therapy
Effects:
-Decreased: (4)
-Increased: (5)
A

Estrogen-only hormone therapy
Effects:

Decreased production/activity:

  • Cholesterol
  • Anti-thrombin III**
  • LH/FSH
  • Osteoclastic activity**

Increased:

  • Triglycerides and HDL-C
  • Clotting factors**
  • Platelet aggregation**
  • Na+/fluid retention
  • Thyroid Binding Globulin (TBG)
81
Q

TQ

5 major points of agreement concerning MHT: (just read)

A
  1. For Younger Women:
    -MHT is an acceptable option for treating moderate to severe menopausal symptoms in relatively young (up to
    age 59 or within 10 years of menopause) and healthy women
  2. For Women with Vaginal Symptoms Only:
    - The preferred treatments are low doses of vaginal estrogen (topical)
  3. For Women with a Uterus:
    - Women who still have a uterus need to take a progestin along with estrogen to prevent uterine cancer
    - Women who have had their uterus removed can take estrogen‐ alone
  4. For Women at Risk of Blood Clots/Stroke:
    - Both estrogen‐alone therapy and estrogen with progestin therapy increases risk of blood clots in legs/lungs
    - Although risks of blood clots and strokes increase with either type of MHT, risk is rare in 50‐59 year‐old age group
  5. For Women at Risk of Breast Cancer:
    - An increased risk of breast cancer seen within 3‐5 years of continuous estrogen with progestin therapy
    - Risk of breast cancer decreases after MHT is stopped
82
Q

Do NOT use MHT in the following women: (4)

A
  • Women with history of breast/ovarian cancer or those with elevated risk (FamHx)
  • Those at risk for osteoporosis
  • For prevention of CHD/CVD
  • To maintain or improve cognitive health or dementia
83
Q

List the 5 SERMs.

A
Tamoxifen
Toremifene
Raloxifene
Ospemifene
Bazedoxifene
84
Q
  • Antagonist at breast
  • Agonist at bone and uterus
  • Increased risk of thromboembolic events and endometrial cancer
  • Used to treat and prevent recurrence of ER/PR (+) breast cancer
A

Tamoxifen (and Toremifene)

85
Q
  • Antagonist at breast and uterus
  • Agonist at bone
  • Increased risk of thromboembolic events, but NO risk of endometrial cancer (vs. tamoxifen)
  • Used primarily to treat osteoporosis
A

Raloxifene

86
Q

Used to treat moderate to severe dyspareunia (painful intercourse):

A

Ospemifene

(However, if the question asks for a hormone therapy for dyspareunia, the answer would be an estrogen cream, NOT ospemifene)

87
Q
  • Used to treat moderate to severe vasomotor symptoms associated with menopause
  • Prevention of post-menopausal osteoporosis
A

Bazedoxifene (with CEE)
(for women with intact uterus)

(cannot use bazedoxifene if estrogen is contraindicated in pt!)

88
Q

Difference between tamoxifen and toremifene in terms of cis/trans conformation and estrogenic activity:

A

Tamoxifen:
-trans = anti-estrogenic

Toremifene:
-cis = estrogenic activity

89
Q

TQ

Toremifene is also shown to promote production of:

A

TGF-ß (an inhibitory growth factor)

therefore if the question talks about the tumor stabilizes but not regressing, change from tamoxifen to toremifene!

90
Q

Non-BC effects of tamoxifen/toremifene: (3)

A
  • Anti-resorptive effect on bone (decrease in vertebral/hip fractures)
  • Decreases TC, LDL, and Lp(a); no change in HDL/TGs; raises Apo-A1 (Toremifene has a more beneficial lipid profile by increasing HDL)
  • Can stimulate endometrial proliferation and thickening
91
Q

MOA:

  • Fxns as an estrogen agonist by binding to ERs in vagina (anti-estrogenic in breast) ->
  • Increases superficial cell growth (on vaginal smear), increases vaginal secretions, decreases vaginal pH, reduces pain-discomfort during vaginal intercourse
  • Stimulatory endometrial effects (use cautiously in women with intact uterus)

SEs: hot flashes/sweating, vaginal discharge, estrogenic effects on coagulation

Which drug?

A

Ospemifene (tx dyspareunia)

92
Q

Ospemifene contraindicated in: (3)

A
  • Vaginal bleeding
  • Stroke/MI/VTE/PE/etc…
  • Estrogen-related neoplasia (e.g., uterine/breast cancer)
93
Q

MOA:

  • Antagonist in endometrium (replaces progestin‐concept in women with an intact uterus)
  • Also estrogenic (agonist) physiological effects (due to CEE component)
A

Bazedoxifene (with CEE)

94
Q

2 anti-estrogen drugs:

A

Clomiphene
Fulvestrant

(Q stem will be built around the indication, then will be asked to pick correct Rx for that indication. Answer will either be one of the above two Rx’s!)

95
Q
  • Antagonist at ERs in hypothalamus
  • Prevents normal feedback inhibition and increased release of LH and FSH from pituitary, which stimulates ovulation
  • Used to treat infertility** due to anovulation (e.g., PCOS)
  • May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances
A

Clomiphene

tx for infertility

96
Q

TQ

  • Anti‐estrogenic on breast cancer cells/tumors
  • Used as treatment of hormone‐receptor(+) breast cancer in tamoxifen‐resistant/failure pts
  • Rx’s structure hinders ER dimerization and increases degradation thereby abolishing ER‐mediated gene transcription (not just a receptor blocker)
  • Tamoxifen not able to do this; therefore this Rx is useful in tamoxifen‐resistant pts**

Which drug?

A

Fulvestrant