Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Myometrial phases (4)

A

Phase 0 = Quiescence (includes 90% of pregnancy)

Phase 1 = Activation

Phase 2 = Stimulation

Phase 3 = Involution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phase 0 = Quiescence

Hormones present at this time?

A

PROGESTERONE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phase 2 = Stimulation

what happens?
what hormones do this (3)

A

LABOR

Hormones:
Prostaglandins
Oxytocin
CRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Uterine tocolytics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PGF2a

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

A

FP → Gq → increase Ca2+ → myometrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Oxytocin binds what kind of receptor?

what happens when it is stimulated?

A

Oxytocin → Gq → increase Ca2+ → myometrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Epinephrine binds what kind of receptor on the uterus? what happens when it is stimulated?
Epi → B2 → Gs → increase cAMP → myometrial relaxation
26
Dinoprostone
synthetic PGE2 ADRs: intestinal cramping, diarrhea, nausea Stimulates cervical effacement (ripening) when applied vaginally
27
Misoprostol
synthetic PGE1 ADRs: fewer systemic side effects Induces uterine contractions
28
Oxytocin (Pitocin) - use? - ADRs (2)
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
Tocolytic Agents: Prostaglandin synthesis inhibitors (indomethacin) - mechanism? - ADRs?
Inhibits COX1 and COX2 ADR: closure of ductus arteriosus in utero can lead to pulmonary HTN postnatally
30
Tocolytic Agents: B2 adrenergic agonists (Terbutaline): - effective for what? - ADRs?
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
Tocolytic Agents: Magnesium sulfate: - mechanism? - use? - ADRs?
Chemical antagonist of Ca2+ NO longer used at UCH as tocolytic Still indicated for pre-eclampsia and eclampsia
32
Tocolytic Agents: Calcium channel blockers (nifedipine) - mechanism? - use? - ADRs?
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
Tocolytic Agents: Ethanol -mechanism?
Inhibits pituitary release of oxytocin No longer used to potential adverse side effects in both mother and fetus
34
Erectile Dysfunction Drugs
phosphodiesterase inhibitors, increase cGMP Sildenafil Vardenafil Tadalafil
35
Malformations
morphologic or structural abnormalities due to an INTRINSICALLY abnormal development process EX) Polydactyly, Syndactyly, single gene/chromosomal disorders
36
Deformations
morphologic or structural abnormalities due to a mechanical force, EXTRINSIC or INTRINSIC EX) Arthrogryposis and club feet secondary to oligohydramnios
37
Disruptions
morphologic or structural abnormalities due to destruction of normally developing tissue
38
Principal causes of human birth defects: (7)
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
how timing of exposure of teratogens impacts human development
Each system has a different critical time period of development Exposure to same teratogen at different times during gestation can cause different effects
40
EX) Congenital Rubella and timing of exposure
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
Phenocopies
similar birth defect phenotype resulting from a genetic versus an environmental/teratogenic cause EX) Isotretinoin exposure very similar to 22q11.2 deletion
42
Development field
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
Hierarchical pathways in human development
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
Threshold theory of environmental/genetic interactions for birth defects
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
Screening Tests
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
MOST screening is _______ Most anomalies occur in ____________
MOST screening is NORMAL MOST anomalies occur in low risk patients
47
Who should you NOT give a screening test to?
Do NOT give screening test for patient if they do not want to accept risks of diagnostic follow up of a positive result
48
Diagnostic Tests
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
Targeted screening
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
Population Screening
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
First trimester screening (11-14 weeks) (3 things)
1) Ultrasound 2) Serum biochemistry: hCG, PAPP-A 3) Maternal factors: age, prior history of aneuploidy, weight, race, number of fetuses
52
First trimester ultrasound looks for what?
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
Second trimester: -Cervical length measurement
After 16 weeks: transvaginal US to measure cervical length and determine risk of preterm delivery
54
3 tests that can estimate gestational age in the second trimester
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
Maternal serum analytes: (4)
AFP Unconjugated estriol hCG Dimeric Inhibin A
56
Alphafetoprotein
made in fetal liver, predominant blood protein in fetus, and cleared by maternal renal function Marker for NTDs (high), Down Syndrome (low)
57
Neural tube defect: AFP? unconjugated estriol? hCG?
*AFP - INCREASED Unconjugated estriol = normal hCG = normal
58
Trisomy 21 AFP? unconjugated estriol? hCG? inhibin A? PAPP-A?
AFP - LOW Unconjugated estriol = low hCG = INCREASED Inhibin A = INCREASED PAPP-A = decreased
59
Trisomy 18 AFP? unconjugated estriol? hCG? PAPP-A?
Trisomy 18 (everything is LOW) AFP - low Unconjugated estriol = low hCG = low PAPP-A = decreased
60
Trisomy 13 what lab value?
PAPP-A = DECREASED
61
Screening tests for fetus: (4)
Maternal serum biochemical screening Ultrasound (1st trimester with nuchal translucency) Ultrasound (fetal anatomy survey) Maternal serum cell free fetal DNA + microarray
62
Maternal serum cell free fetal DNA
Noninvasive test with no miscarriage risk High sensitivity and specificity Available early in gestation Used for patients at increased risk for aneuploidy
63
Diagnostic tests for the fetus: (2)
Chorionic villus sampling (around 10-13 weeks) Amniocentesis (performed after 15 weeks)
64
Chorionic villus sampling
(around 10-13 weeks) Detects genetic, metabolic, and DNA abnormalities Done earlier than amniocentesis

Life Cycles (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions