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Life Cycles > Week 7 > Flashcards

Week 7 Flashcards

1
Q

Labor

A

effective uterine contractions leading to dilation and effacement of the cervix and delivery of the fetus

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2
Q

Clinical Stages of Labor: (4)

A

1) Effective contractions to complete dilation of cervix
2) Complete dilation to delivery of fetus
3) Delivery of fetus to delivery of placenta
4) First 6 hours after delivery

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3
Q

The first clinical stage of labor is made up of what 2 sub-phases?

A

First stage = Effective contractions to complete dilation of cervix

  • Initial latent phase → contractions without cervical change
  • Active phase → acceleration and deceleration phase in cervical dilation
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4
Q

Uterus during pregnancy:

undergoes 3 main changes

A

1) Growth by hyperplasia and hypertrophy
- Weight increases from 50g → 1000g

2) Increased connectivity of myocytes (connexins)

3) Increased oxytocin receptors (modulate calcium movement)
- Receptors most concentrated at fundus (top of uterus)

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5
Q

What is the function of the gap junctions between myocytes in the uterus?

A

Increased connectivity of myocytes (connexins)

Cells connected by gap junctions via connexin 43

Electrochemical and mechanical coupling

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6
Q

Molecular/Cellular mechanisms of myometrial quiescence: (5)

A

LOW Ca2+, LOW PG, LOW oxytocin

1) Membranes: produce prostaglandin dehydrogenase (breaks down PG)
2) Myometrium: myosin and actin not arranged properly for contraction
3) Progesterone secreted → anti-inflammatory and NO production → increase cGMP → reduce MLCK activity
4) CRH → receptor mediated increase in cAMP signal → PKA → shut down MLCK activity
5) K+ channels open (maintain negative potential in cell) and Na/K+ ATPase

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7
Q

Molecular/Cellular mechanisms of myometrial ACTIVATION phase (5)

A

1) Add gap junctions
2) Express L-type calcium channels to allow Ca2+ in
3) Express oxytocin receptors
4) Express COX (increase PG production) - BUT still have PGDH, so no increase in PG yet
5) Express prostaglandin receptors

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8
Q

Molecular/Cellular mechanisms of myometrial CONTRACTION phase (4)

A

1) New CRH receptor that promotes CONTRACTION
CRH → PKC → promote contractility

2) Stop production of PGDH → increase PG
3) PG → internal Ca2+ release
4) Oxytocin binds → depolarize cell and allow Ca2+ in

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9
Q

Myometrial phases (4)

A

Phase 0 = Quiescence (includes 90% of pregnancy)

Phase 1 = Activation

Phase 2 = Stimulation

Phase 3 = Involution

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10
Q

Phase 0 = Quiescence

Hormones present at this time?

A

PROGESTERONE

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11
Q

Progesterone

  • source
  • function?
  • expressed during what phase?
A

myometrial inhibitor, quiescence factor in early pregnancy

Source = placenta

Function:

  • Block myosin light chain kinase
  • Inactivates prostaglandins, decreases inflammation signaling

Expressed during quiescent phase (also expressed during contraction but acts on a different receptor)

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12
Q

Phase 1 = Activation

what is the purpose of this phase?

-what is hormones and signals are modulating this? (3)

A

Molecular changes in myometrium without labor - getting ready to contract

Hormones and modulators:

1) ESTROGEN mediated activation factor
2) Uterine stretch
3) Fetal signals

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13
Q

Phase 2 = Stimulation

what happens?
what hormones do this (3)

A

LABOR

Hormones:
Prostaglandins
Oxytocin
CRH

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14
Q

Prostaglandins (role in labor?)

Source?
Function?

A

stimulates contractions (PGE2, PGF2a)

Source = myometrium and placental membranes

Mechanism:

  • Paracrine function
  • Increases intracellular calcium
  • Facilitates weakening of amnion and chorion
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15
Q

Oxytocin

source?
function?
mechanism?

A

myometrial stimulant

Source = maternal anterior pituitary

  • Stimulates contractions
  • Differential distribution on uterus - highest concentration at fundus

Mechanism: increases intracellular Ca2+, activates myosin light chain kinase

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16
Q

CRH

function in labor?
source?
A

myometrial inhibitor (maintains quiescence) AND induces labor acting as a myometrial stimulant

Source = Placenta

Shift between quiescence and contractile function due to shift in receptor isoforms
Important for pulmonary maturation on fetal side

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17
Q

Fetal CRH system

A

POSITIVE feedback system:

CRH produced by baby pituitary → ACTH → fetal adrenal → fetal cortisol → feed FORWARD to have exponential increase in fetal CRH

Driven by fetal maturation

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18
Q

Phase 3 = Involution

what happens?
what two hormones do this?

A

Get uterus back to normal size and prevent bleeding

Hormones:
Oxytocin
Inflammatory cell activation

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19
Q

Structure of Cervix:

what happens to this structure as you approach labor?

A

Connective tissue (made up of collagen and proteoglycans)

Proteases degrade collagen and proteoglycans + edema later in pregnancy during cervical ripening

Smooth muscle of internal os (holds baby in)
→ Dilates passively with contractions

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20
Q

Uterine tocolytics: (6)

A

1) Calcium antagonists (Nifedipine)
2) Oxytocin receptor antagonists (Atosiban)
3) Inhibitors of PG synthesis (indomethacin)
4) NO donors (nitroglycerin)
5) Beta-mimetics (Fenoterol, terbutaline, ritodrine)
6) Magnesium

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21
Q

Uterine tocolytics

A

“treatment” for preterm labor - only delay about 48 hrs, done so that full course of steroids can be given

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22
Q

PGE2-PGE1: targets in labor? (2 receptors and what happens when they are stimulated?)

A

EP1 (myometrium) → Gq → increase Ca2+ → myometrial contraction

EP2,3,4 (cervix) → Gs → increase cAMP → cervix ripening-dilation

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23
Q

PGF2a

target in labor? (receptor and what happens when stimulated?)

A

FP → Gq → increase Ca2+ → myometrial contraction

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24
Q

Oxytocin binds what kind of receptor?

what happens when it is stimulated?

A

Oxytocin → Gq → increase Ca2+ → myometrial contraction

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25
Q

Epinephrine binds what kind of receptor on the uterus?

what happens when it is stimulated?

A

Epi → B2 → Gs → increase cAMP → myometrial relaxation

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26
Q

Dinoprostone

A

synthetic PGE2

ADRs: intestinal cramping, diarrhea, nausea

Stimulates cervical effacement (ripening) when applied vaginally

27
Q

Misoprostol

A

synthetic PGE1

ADRs: fewer systemic side effects

Induces uterine contractions

28
Q

Oxytocin (Pitocin)

  • use?
  • ADRs (2)
A

Augment uterine contractions

Used for labor induction AFTER cervical ripening

Also effective for postpartum hemorrhage

ADRs:
Water intoxication (similar to ADH)
Uterine rupture and impaired fetal oxygenation

29
Q

Tocolytic Agents:

Prostaglandin synthesis inhibitors (indomethacin)

  • mechanism?
  • ADRs?
A

Inhibits COX1 and COX2

ADR: closure of ductus arteriosus in utero can lead to pulmonary HTN postnatally

30
Q

Tocolytic Agents:

B2 adrenergic agonists (Terbutaline):

  • effective for what?
  • ADRs?
A

Higher incidence of maternal side effects (jitteriness, hypokalemia, hyperglycemia, hypotension)
→ infant hypoglycemia

Effective at suppressing contractions - treating premature labor

Less effective if cervix dilated and membranes have ruptured

31
Q

Tocolytic Agents:

Magnesium sulfate:

  • mechanism?
  • use?
  • ADRs?
A

Chemical antagonist of Ca2+
NO longer used at UCH as tocolytic
Still indicated for pre-eclampsia and eclampsia

32
Q

Tocolytic Agents:

Calcium channel blockers (nifedipine)

  • mechanism?
  • use?
  • ADRs?
A

Used at 32-34 weeks

Fewer maternal side effects than MgSO4 or B-agonists

Potential concern that fall in maternal BP may reduce blood flow between uterus and placenta

33
Q

Tocolytic Agents:

Ethanol

-mechanism?

A

Inhibits pituitary release of oxytocin

No longer used to potential adverse side effects in both mother and fetus

34
Q

Erectile Dysfunction Drugs

A

phosphodiesterase inhibitors, increase cGMP

Sildenafil
Vardenafil
Tadalafil

35
Q

Malformations

A

morphologic or structural abnormalities due to an INTRINSICALLY abnormal development process

EX) Polydactyly, Syndactyly, single gene/chromosomal disorders

36
Q

Deformations

A

morphologic or structural abnormalities due to a mechanical force, EXTRINSIC or INTRINSIC

EX) Arthrogryposis and club feet secondary to oligohydramnios

37
Q

Disruptions

A

morphologic or structural abnormalities due to destruction of normally developing tissue

38
Q

Principal causes of human birth defects: (7)

A

1) Chromosomal aberrations = 10-15%
2) Mendelian inheritance = 2-10%

3) Maternal/placental infections = 2-3%
- (Toxoplasmosis, Rubella, CMV, HIV, Syphilis)

4) Maternal disease states = 6-8% - (Diabetes, PKU, Endocrinopathies)
5) Drugs and chemicals = 1% - (Alcohol, folic acid antagonists, androgens, phenytoin, thalidomide, warfarin, 13-cis-retinoic acid)

6) Multifactorial = 20-25%
EX) Neural tube defects

7) Unknown = 40-60%

39
Q

how timing of exposure of teratogens impacts human development

A

Each system has a different critical time period of development
Exposure to same teratogen at different times during gestation can cause different effects

40
Q

EX) Congenital Rubella and timing of exposure

A

First trimester → congenital heart defects, deafness, neuro defects, retinopathy

Second or third → more likely to avoid serious systemic defects and only get localized inflammatory and destructive lesions

41
Q

Phenocopies

A

similar birth defect phenotype resulting from a genetic versus an environmental/teratogenic cause

EX) Isotretinoin exposure very similar to 22q11.2 deletion

42
Q

Development field

A

groups of embryonic structures that respond as a single developmental unit

  • Tissue sharing gene expression (hedgehog signaling pathway)
  • Tissues related to each other through location (branchial arches)
  • Tissues sharing developmental timing (embryonic inner cell mass)
  • Tissues affected by interacting processes (cell proliferation and apoptosis)
43
Q

Hierarchical pathways in human development

A

Cascades of genes that all has to happen at the right time and in the right tissue

Involves cell migration, cell division, interaction between tissue types, controlled cell death

44
Q

Threshold theory of environmental/genetic interactions for birth defects

A

Liability = all genetic and environmental factors that influence the development of a multifactorial disorder

Influenced by genetic predisposition, sporadic gene causes, mechanical disruption, etc.

Gene/environment interaction “shifts” threshold of liability

Can “shift” the threshold with supplementation of folic acid

45
Q

Screening Tests

A

assess risk, quick, noninvasive, widely accessible, high NPV, low false positives, first step only - pre and post test counseling

Done to reassure families at risk and prepare for the birth of a baby with anomalies

Develop plans for monitoring and for neonatal care

Provide data to allow continuation decision making

**Cannot known positive predictive value unless you know the PREVALENCE of disorder

46
Q

MOST screening is _______

Most anomalies occur in ____________

A

MOST screening is NORMAL

MOST anomalies occur in low risk patients

47
Q

Who should you NOT give a screening test to?

A

Do NOT give screening test for patient if they do not want to accept risks of diagnostic follow up of a positive result

48
Q

Diagnostic Tests

A

as close to truth as possible, maybe longer or invasive, may require special training, gives a diagnosis if completed

Last or first step

Risks and pre/post test counseling

49
Q

Targeted screening

A

Screen with history, exam, routine labs, or other data

Examine highest risk subgroups, especially for rare diseases

Could be screen-in or screen-out

Counseling issues are the same

50
Q

Population Screening

A

Everyone screened to identify disease or disease risk

Can be opt-out

EX) neonatal metabolic screening

Offer screening or diagnosis to all for fetal evaluation - can opt out

51
Q

First trimester screening (11-14 weeks) (3 things)

A

1) Ultrasound
2) Serum biochemistry: hCG, PAPP-A
3) Maternal factors: age, prior history of aneuploidy, weight, race, number of fetuses

52
Q

First trimester ultrasound looks for what?

A

1) 82-87% detection of Down Syndrome
- 5% screen positive
- Larger NT is higher risk and higher risk of other anomalies
- Nasal bone adds additional sensitivity

2) Crown → rump length helps determine age*

+/- 1 week in first trimester = MOST ACCURATE

53
Q

Second trimester:

-Cervical length measurement

A

After 16 weeks: transvaginal US to measure cervical length and determine risk of preterm delivery

54
Q

3 tests that can estimate gestational age in the second trimester

A

1) Biparietal Diameter
2) Abdominal circumference
3) Femur length

Take all of these things and use them to estimate fetal weight

+/- 2 weeks in second trimester
+/- 3 weeks in 3rd trimester

55
Q

Maternal serum analytes: (4)

A

AFP

Unconjugated estriol

hCG

Dimeric Inhibin A

56
Q

Alphafetoprotein

A

made in fetal liver, predominant blood protein in fetus, and cleared by maternal renal function

Marker for NTDs (high), Down Syndrome (low)

57
Q

Neural tube defect:

AFP? unconjugated estriol? hCG?

A

*AFP - INCREASED
Unconjugated estriol = normal
hCG = normal

58
Q

Trisomy 21

AFP? unconjugated estriol? hCG? inhibin A? PAPP-A?

A

AFP - LOW

Unconjugated estriol = low

hCG = INCREASED

Inhibin A = INCREASED

PAPP-A = decreased

59
Q

Trisomy 18

AFP? unconjugated estriol? hCG? PAPP-A?

A

Trisomy 18 (everything is LOW)

AFP - low

Unconjugated estriol = low

hCG = low

PAPP-A = decreased

60
Q

Trisomy 13

what lab value?

A

PAPP-A = DECREASED

61
Q

Screening tests for fetus: (4)

A

Maternal serum biochemical screening

Ultrasound (1st trimester with nuchal translucency)

Ultrasound (fetal anatomy survey)

Maternal serum cell free fetal DNA + microarray

62
Q

Maternal serum cell free fetal DNA

A

Noninvasive test with no miscarriage risk

High sensitivity and specificity

Available early in gestation

Used for patients at increased risk for aneuploidy

63
Q

Diagnostic tests for the fetus: (2)

A

Chorionic villus sampling (around 10-13 weeks)

Amniocentesis (performed after 15 weeks)

64
Q

Chorionic villus sampling

A

(around 10-13 weeks)

Detects genetic, metabolic, and DNA abnormalities

Done earlier than amniocentesis

Life Cycles (8 decks)

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