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Phys & Pharm Flashcards

1
Q

Considerations in using valproic acid in pregnancy

A

Don’t do it

Formerly category X for migraine prevention and D for epilepsy, demonstrating that one med can have different categorizations based on use

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2
Q

Give 4 factors that play into teratogenicity of a substance

A

Timing
Dose
Duration of exposure
Genetic susceptibility of mother and fetus (esp true of EtOH)

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3
Q

Your patient had an exposure to a teratogenic medication before she knew she was pregnant. How should she be counseled in regards to likelihood of a congenital defect due to the exposure?

A

Baseline (no exposure) risk of congenital defect = 3-4%

Medication exposures account for <1% of birth defects
(Just because there has been an exposure does not mean that there WILL be a defect - can be reassuring to parents considering terminating an early pregnancy)

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4
Q

Give 8 examples of drugs/classes that were discussed as teratogens

A
  • ACE-i (ex: lisinopril)
  • Quinolones (controversial; ex: cipro)
  • Tetracyclines (ex: doxycline)
  • Isotretinoin (vit A derivative)* High risk
  • Lithium
  • Thalidomide (not used much anymore)
  • Carbamazepine
  • Valproic acid
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5
Q

What are some drugs that affect uterine contractility?

A
  • M3 agonists (glaucoma meds, ie pilocarpine – stimulate contractions)
  • A-agonists (decongestants – stimulate contractions)
  • Prostaglandins (ex: misoprostol – stimulate contractions)
  • B2 agonists (bronchodilators – uterine relaxation)
  • CCBs (ex: amlodipine – uterine relaxation)
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6
Q

How might drugs need to be changed/monitored during pregnancy?

A

Some drugs require closer monitoring than others, such as:

  • Anticonvulsants
  • Lithium
  • Thyroid meds

Because the blood volume increases dramatically, the volume of distribution also increases so we may need to increase dose in 3rd trimester in order to be in the therapeutic window.

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7
Q

Name 3 pharmokinetic/dynamic changes that occur in pregnancy

I honestly don’t remember the difference between kinetics and dynamics anymore, sorry Cuddy

A
  • Increased renal clearance
  • Increased free fraction
  • Increased Vd
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8
Q

Name three characteristics that makes a substance more likely to cross the placenta

A
  • Low molecular weight
  • Free (not protein bound)
  • Weakly basic (fetal pH is more acidic; drug will ionize and not diffuse back across placenta)
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9
Q

What are the 1st and 2nd line Tx’s for nausea and vomiting in pregnancy?

A

1st: non-pharm: Diet changes
2nd: Vitamin B6 and antihistamines (ex: meclizine)

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10
Q

What are the 1st and 2nd line Tx’s for HA in pregnancy?

A

1st: non-pharm
2nd: Acetominophen

(Avoid NSAIDs because they can result in premature closure of the PDA and are CIx in the third trimester)

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11
Q

What is the 1st line Tx for pre-existing HTN in a pregnant patient?

A

Labetalol or nifedipine

If a woman is not on contraceptives/is trying to conceive, try to get her HTN stabilized on something OTHER than an ACE-i well before pregnancy

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12
Q

What are the 1st and 2nd line Tx’s for pre-existing DM (type II) in pregnancy?

A

1st: non-pharm
2nd: Insulin/metformin

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13
Q

What is the 1st line Tx for depression in pregnancy?

A

SSRI, not paroxetine (ex: sertraline)

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14
Q

What is the 1st line Tx for bipolar disorder in pregnancy?

A

Lithium + antipsychotics with close monitoring of lithium especially

NO valproic acid or carbamazepine

Must treat but do so carefully.

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15
Q

What is the 1st line treatment for epilepsy in pregnancy?

A

Important that these patients try to stabilize on monotherapy before conception (suggest LARC until stabilized). Polytherapy ass’d with cognitive defects.

Lamotrigine or levetiracetam preferred

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16
Q

What is a consideration in treating bipolar disorder in a postpartum woman?

A

Lithium, used to treat bipolar, concentrates highly in the breast milk. Don’t use it if possible.

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17
Q

How do we determine the extent of exposure that an infant experiences via breast milk?

A

We compare the amount that is in the baby to the amount that is in mom.

To figure out amount in baby:
(concentration in milk x quantity of milk consumed) / baby weight

To figure out amount in mom = plasma concentration / mom weight

If the ratio (milk:mom) is >1, the drug is concentrating highly in the breast milk (ex: lithium)

*Basically we want less drug per pound in baby than in mom.

If the ratio is low, the drug is not concentrating highly. We consider <10% safe. Most wind up being <1%.

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18
Q

What are some drug classes that can decrease milk production?

A 
Dopamine agonists (bromocriptine)
A-agonists (decongestants)
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19
Q

What are some drugs that can increase milk production?

A

Dopamine antagonists, such as some antipsychotics and antiemetics

20
Q

What’s an important consideration when treating pain in a breastfeeding woman?

A

Morphine is safer than codeine: codeine metabolizes to morphine IN the breast milk, giving the infant a megadose of morphine, while morphine is metabolized by mom first, resulting in less exposure to the infant

21
Q

If you were to look at a fetal oocyte ~8-9 weeks gestation, in what phase of replication would that oocyte be?

A

Arrested in Prophase 1 of Meiosis I

22
Q

If you were to look at an unfertilized oocyte of a post-pubertal woman, in what phase of replication would that oocyte be?

A

Arrested in Metaphase 2 of Meiosis I

23
Q

When does Meiosis II occur for an oocyte?

A

Upon fertilization

24
Q

What receptors are present on Theca cells, and what do these cells do? What enzymes are necessary here?

A

LH receptors

Cholesterol –> pregnenolone -> progesterone –> androgens

17a-hydroxylase and/or 17,20 lyase enzymes are required

25
Q

What receptors are present on Granulosa cells, and do these cells do? What enzymes are necessary here?

A

FSH and LH receptors

Cholesterol –> pregenolone –> progesterone
(no androgen formation!!!)

Androgens –> estrogens via aromatase

26
Q

Estrogen increases the expression of LH (and FSH) receptors on granulosa cells. What is the mechanism of this increase and how is it helpful?

A

cAMP is a byproduct of estrogen production, so more estrogen = more cAMP

cAMP stimulates expression of LH receptors on granulosa cells

More LH receptors means more progesterone can be created (and then shuttled to theca cells to make androgens), allowing more estrogen to be made.

27
Q

Considering an average 28 day cycle, describe the levels of E2, Progesterone, LH and FSH in relation to each other on day ~8

A

E2 will be high
Progesterone will be low
FSH is dropping due to negative feedback from E2
LH is lower than FSH

28
Q

Considering an average 28 day cycle, describe the levels of E2, Progesterone, LH and FSH in relation to each other on day 14

A

Super high E2 caused a surge in LH which triggered ovulation

E2 is higher than progesterone; LH is higher than FSH

29
Q

Considering an average 28 day cycle, describe the levels of E2, Progesterone, LH and FSH in relation to each other on day ~20

A

Progesterone and E2 are being produced by the corpus luteum and are very high (P > E2)

FSH > LH; both have dropped significantly due to negative feedback

30
Q

If there is a surge in LH > FSH, what hormones will be produced in higher expression?

A

Progesterone and androgens > estrogens

31
Q

Describe some actions of progesterone

A

Increases endometrial secretions during luteal phase
Increases sexual desire
Increases progesterone receptors
DECREASES E2 receptors
Antagonizes mineral corticoid receptors (decreased Na+ reabsorption; withdrawal = bloating)

32
Q

If you were to run endocrine labs on a postmenopausal woman, how would you expect values to compare to a premenopausal woman?

A 
Low inhibin
Low E2
Low progesterone
High LH
High FSH
High androstendione/T
33
Q

Describe the shunts of fetal circulation

A
  1. ) Placenta: umbilical vein –> liver; mixes mom’s arterial blood with fetal venous blood
  2. ) Ductus venosus: Liver –> inferior vena cava; mixes umbilical blood with fetal venous blood
  3. ) Ductus arteriosus: Pulmonary vein –> aorta. Protects against right-sided atrophy and is kept open by high pulmonary pressures.
  4. ) Foramen ovale: RA –> LA. Allows blood to bypass lungs. Protects against right-sided atrophy and is kept open by high pulmonary/right-sided pressures.
34
Q 
Touchberry will probably have a little graph thing to map out pulmonary changes in the neonate after birth.
What happens to:
 -- Pulmonary vascular resistance
 -- Pulmonary blood flow
 -- PaO2
 -- Pulmonary vasodilation
 -- Pulmonary pressure (MAPpulm)
A
    • Pulmonary vascular resistance = DOWN
    • Pulmonary blood flow = UP
    • PaO2 = UP
    • Pulmonary vasodilation = UP
    • Pulmonary pressure (MAPpulm) = DOWN
35
Q

What is one of the major changes that occurs in the alveoli immediately after birth?

A

Epinephrine (along with O2, glucocorticoids, and other substances) cause insertion of more ENACs in the alveoli.

This allows Na+ to enter the alveoli from the lungs, pulling water along.

Water then exits the alveoli into the interstitium (out of lungs) via passive and paracellular transport

36
Q

What are the major threats to the neonate and what are the basic defenses against these threats?

A
  • Hypoxia: Crying helps open airway/allows mouth breathing
  • Hypoglycemia: Immediate breast feeding + increased glucagon, epi, and decreased insulin –> gluconeogenesis
  • Hypothermia: Most important is non-shivering thermogenesis
37
Q

Describe the process of non-shivering thermogenesis

A
  • Process relies on brown fat

Cold temps trigger release of T4 and epi
– T4 –> T3, necessary for upregulation of UCPs (action of epi is also necessary for this upregulation)

– Epi: GPCR –> adenylyl cyclase –> ATP –>cAMP –> PKA
Converts triglycerides to free fatty acids
Also goes through a cascade involving PKA and 5’iodinase that assists T3 in upregulating UCPs

The important part:
T3 + epi cause uncoupling proteins to be expressed and inserted into mitochondria, and also result in the conversion of free fatty acids. The FFA diffuse into the mitochondria and are used for thermogenesis.

38
Q

In what tissues are a-estrogen receptors found?

A

Breast
Endometrium
Hypothalamus

39
Q

In what tissues are B-estrogen receptors found?

A

Bone
Brain
Endothelial cells
Granulosa cells

40
Q

How does tamoxifen interact with estrogen receptors?

A

Antagonist at a-receptors in the breast

Agonist at B-receptors in the bone

41
Q

How does raloxifeine interact with estrogen receptors?

A

Antagonist in in breast, uterus, and CNS

Agonist in bone

42
Q

Why does bloating occur in the premenstrual phase?

A

Progesterone acts as an antagonist at mineral corticoid receptors:

  • When it is high, it prevents aldosterone from increasing Na+ reabsorption = less Na+ reabsorption = less water retention
  • In the premenstrual phase, progesterone plummets. The withdrawal of progesterone then allows aldosterone to cause more retention of Na+ and thus more retention of water.
43
Q

Which contraceptive method increases rates of functional ovarian cysts?

A

POPs

44
Q

What are the contraceptive methods we discussed that include estrogen? Which are progestin-only?

A

Combo (include estrogen) = COC, patch, and ring

All others are progestin-only: POP, DMPA, implant, IUD, and emergency contraception

(Except paragard/copper IUD = non-hormonal)

45
Q

What is the first line treatment for urinary incontinence?

A
  • Manage co-existing diseases/risk factors
  • Address fluid intake
  • Bladder training/Kegels
46
Q

What is the second-line treatment for urinary incontinence?

A

Medications: 2 classes:

  • Antimuscarinics: oxybutinin, toviaz. USE XR VERSIONS. #1 complaint is dry mouth
  • B3 agonist: Mirabegnon: do not use in patients with uncontrolled HTN
47
Q

What are the third-line treatments for urinary incontinence?

A

More invasive procedures:

  • Surgical sling
  • Interstim (S3)
  • Botox for urge incontinence

WH (2 decks)

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