placenta Flashcards
(82 cards)
1
Q
The placenta is the major lifeline between the mother & the fetus.
What are the roles
A
- Supplies nutrients to the fetal gut
- Exchanges O2 and CO2 in fetal lung
- Helps fetal kidney regulate fluid volume and dispose wastes
It is a endocrine. gland that. can make steroids and proteins that. can affect. mom and bby metalism
2
Q
what. is the mature placenta made up of?1
A
- chorionic villi
- intervillous space
- decidua basalis
3
Q
functional unit of the placenta
A
• Chorionic villi- > branches alot to incrase SA for maternal-fetal exhcnage
4
Q
what. is the purpose of intervillous space
A
Spiral arteries from mom empty into intervillous spaces, which is drained by maternal veins
5
Q
what is the maternal. blood flow
A
- Pulses. of maternal blood -> uterus -> intervillous spaces via spiral arteries.
- After bathing choronic villus, blood returns through veins in the decidua basalis -> uterine and pelvic veins.
INTERVILLOUS SPACE SERVES AS OUR FUNCTIONAL CAPILLARY: THERE. ARE NO CAPILLARIES BETWEEN MOM A. and V.
6
Q
Factors regulating maternal blood flow
A
- maternal arterial BP
- intra-uterine pressure
- uterine contraction
7
Q
how does uterine contractions affect maternal flow?
A
Uterine contractions slow arterial flow into the intrachorionic space and completely stop venous return.
RESULT: More blood within the intervillous space to provide continuous but reduced exchange.
8
Q
What is the fetal blood flow?
A
- 2 Umbilcal arteries (O2 poor blood) -> placenta, where fetal blood is oxygenated -> umbilical vein (O2 rich blood) -> fetus
9
Q
• Two important functions of the amniotic fluid:
A
- Buffer to protect fetus from external, physical insults
- Excretes wastes of the fetus.
10
Q
Describe gases move across the placenta
A
- Maternal blood that enter intervillous space has a gas composition similar to systemic blood (PO2= 100mm, PCO2= 40mm, pH of 7.4)
- –> goes into choronic villus
- PO2 of blood in intervillous spaces falles (average= PO2= 30-35 mmHg)
The PO2 of the umbilical vein is even less.
11
Q
Blood in the intervillous space has ____ O2, but fetal Hb has a ____ affinity for O2.
A
LOW O2,
HIGH AFFINITY FOR O2
12
Q
Despite the relatively low PO2 of the maternal blood in the intervillous space,
HOW DOES the fetus does not suffer from a lack of O2
A
Fetal Hb has a much higher affinity. for O2 than maternal Hb, and thus, can extract O2 from maternal Hb.
13
Q
Other mechanisms of ensuring that. our fetus gets enough O2!
A
- CO of mom increases per unit body weight of fetus,
- Hb concentration increases -> increasing O2 carrying capacity of fetal blood late in pregnancy
14
Q
Movement across the placenta
- Waste products: urea & creatinine:
- Lipid-soluble steroid hormones:
- Glucose:
- Amino acids:
- Vitamins & minerals:
- Low-density lipoproteins (LDL), transferrin, some hormones, & antibodies (e.g., immunoglobulin G):
A
- Passive movement from fetus -> mom
- Simple diffusion among mom, placenta and fetus
- Facilitated diffusion from mom-> fetus
- AA: secondary active transport
- Vitamines and minerals: active transport
- receptor-mediated endocytosis; plancenta takes up large molcules from mom and uptake will increase throughout gestation until just b4 birth.
15
Q
The__________ of the placenta makes several steroid & protein hormones
A
syncytiotrophoblasts
16
Q
Endocrine fx of placenta (5)
A
1. maintain pregnancy
2. cause lobuloalveolar growth.and function of moms tits
2. Helps bbs metabolism and physiology adapt. a it grows
4. regulate development
5. regulate timing and progression of partutiriton
17
Q
Describe the maternal serum levels during pregnancy for the following hormones and
their physiological functions:
HCG
A
- This is the first hormone produced by the synctioblasts of placenta during pregnancy. It helps maintain pregnancy by binding to LH receptors on the corpus luteum with high affinity to keep up the leuteal progesterone.
- hCG has been associated with morning sickness.
18
Q
Describe the maternal serum levels during pregnancy for the following hormones and
their physiological functions:
Human placental lactogen (HPL)
A
. Detecxted by in synctiotrophoblast by 10 days after conception, in mom blood by 3 weeks and risees PROGESSIVELY t/o pregnancy.
- Simular to GH and prolactin: anabolic and lipolytic
- Antagonistic to insulin and can cause DB in pregnancy by preventing maternal glucose uptake -> increasing glucose for bb.
- Lipolytic: mom then uses energy. from FFA.
19
Q
Primary action of HCG is to stimulate LH receptors on the corpus luteum. What. does it do?
A
- Prevent luteolysis
- Maintains a high level of progesterone during FIRST 10 WEEKS -> peaks. declines at a constant. level
20
Q
Progesterone
A
Placeneta makes a shit ton of progesterone (UNREGULATED) and released mainly into mom. This is needed to maintain dormant myometrium and pregnant.
21
Q
how much progesterone is made by. placenta
draw
A
- unregulated; it makes as much as the supply of cholesterol and levels of cholesterol desmolase and 3B-HSD allows.
- levels continue t/o pregnancy
22
Q
estrogen
Made by: ______
how is it present in body?
A
Made by: syncytiotrophoblasts.
DHEA -> converted by syncytiotrophoblasts -> estradoil 17B, estrone or estriol
23
Q
Fxs of estrogen
A
- increase uteroplacental BF.
- Enhance LDL receptor expression in syncitiotrophoblasts
- Induce prostaglandins & oxytocin receptors
- Promote. growth. of endometrium.
- growth & development of the mammary glands
24
Q
What do the synciotdtropblasts need to make progesterone?
A
CYP11A1 (cholesterol -> pregnenolone)
sTAR protein is NOT required
3B-HSD (pregnenolone -> progesterone)
25
Just before ovulation, the ovary is in the late follicular stage & produces
high levels of estrogen.
## Footnote
**Estrogen promotes**
**1. Growth of uterine endometrium**
**2. Expression of progesterone receptor**
26
The events between _fertilization_ & _implantation_ take ~ ____ days to complete, & implantation occurs at ~ day ___ of the menstrual cycle
– The ovary is in the _______ phase; secretes large amounts of \_\_\_\_\_\_
**6**
**21**
**mid-luteal phase**; secetes large amounts of **progesterone**
27
**how does p_rogesterone help during pregnancy_**
1. _Stimulates secretion from mom uterine glands_, which provide nutrients to the embryo (histotrophic nutrition)
2. Inhibits myometrial contraction and prevents release of paracrine factors the cause period.
3. Progesterone induces the **“window of receptivity”** in the uterine endometrium, which exists from ~ day 20 – 24 of the menstrual cycle (makes the endometrium recetive to implantation)
28
**(histotrophic nutrition)**
What is this
important mode of maternal-to fetal transfer of nutrients for about the 1st trimester of pregnancy, after which it is replaced by **hemotrophic nutrition**
**BBY RLIES ON THIS TO. GET NUTRIENTS. 4 FIRST MONTh**
29
What is the **uterine endometrium** like during implantation
**1. Full thickness**
**2. Actively secretory**
**3. Can tightly adhere embryo**
**4. well vascularized;**
* **efficiently delivering progesterone to endometrium and**
* **captures hCG -\> takes it to ovary -\> rescues corpus luteum.**
30
During pregnancy, **what happens to levels of progesterone and estrogen?**
progesterone & estrogens rise to levels that are **substantially higher than their peak**s in a normal cycle
31
**Elevated levels of progesterone are necessary for _maintaining_ pregnancy.**
Why?
**1. reduces uterine motility**
**2. inhibits propagation of contractions**
32
**• Elevated levels of progesterone & estrogens in pregnancy are achieved by:**
1. Until week 8: **hCG resues corpus leuteum** and is the major source of progesterone and estrogen.
2. By 8 weeks: **placenta** is the major source.
33
After 8 weeks of gestation, __________________ maintains high levels of progesterone & estrogens
**mom-placenta-fetus unit**
## Footnote
**_placenta cant do it alone._**
**needs moms and bbs help**
34
After 8 weeks of gestation, **mom-placenta-fetal unit** maintains high levels of progesterone & estrogens.
Why cant the placenta. do it on its own?
1. cant make enough **cholesterol**
2. Doest have **[17a-hydroxylase and 17-20 desomlase**] to make _estrone_ and _estradoiL_
3. doesnt have **[16a-hydroxylase]** to make _estriol_.
35
The **maternal-placental-fetal unit** overcomes these placental limitations in 2 ways:
what. r they
1. **Mom** brings the **cholesterol** via LDL.
2. **Fetal** adrenal gland and liver have the **3 lacking ezymes, which will DHEA-S**
36
if the fetus has the 3 enzymes to make **estrogen**, does it make some. by itself?
**NO. IT DOES NOT AND SHOULD NOT.**
**1. Lacks _(3β-HSD) & aromatase_, needed to make estrone (estradoil precursor)**
**SHOULD NOT BC:**
**fetus would make a high level of hormones, _which the MOM needs_, NOT fetus**
37
The fetus avoids exposure to dangerously high levels of hormones bc it lacks _3β-hydroxysteroid dehydrogenase (3β-HSD) & aromatase. **How else does it to do?**_
* 1. Placenta is a captures weak androgens fetus makes to prevent masculatinzation.
* 2. Fetus will congute necessary steroids with sulfate, which reduces their activity.
* Pregnenolone that. moves from placenta -\> fetus: sulfinateD. -\> DHEA-S.
* WHEN IT LEAVES THE PLACENTA, DE. SULFN=INATED
38
Fetus will sulfinate things inside of it to reduce activity and prevent exposure. to dangerous hormones. **do they. stay. sulfinated?**
No.
1. when DHEA-S & 16α-hydroxy-DHEA-S move to the placenta, they. are desulfinated.
2. Placenta can has 3B HSDH and aromatose make estrogens -\> **transfer to mom, WHO NEEDS IT.**
39
what is rthe maternal response to pregenancy?
draw
1. **CO and BV increase by 40-50%** in mom during pregnancy.
* -BV begins to increase during f_irst trimester_ SLOWLY. (1-12 weeks)
* -Increases RAPIDLY during _2nd trimester_ (13-26)
* -Increases at a lower rate during 3rd trimester (27-40).
* -Plateus last several weeks.
40
Maternal response to pregnany: Increaes **CO/BF by 40-50%.**
## Footnote
**What mediates increase?**
RAAS secretes **_aldosterone_**, causing reabsoprtion of **_salt_ and _water_.**
41
Both maternal cardiac output & blood volume increase during pregnancy. Increased blood volume results in an **increase in heart rate** (15 beats/min more than usual), **stroke volume**, & . Despite the large increase in plasma volume, **mean arterial pressure (MAP)** usually
1. **Decreases** during **mid-pregnancy** d.t decrease peripheral vascular resistance d/t vasodilation of progesterone and estradoil.
2**. Increases at third trimester,** remaining normal or lower than normal
42
when does CO increase most during pregnancyt?
and why
**1st trimester (INCREASES BY 35-40)**
**ONLY SLIGHLY AT 2ND AND 3RD (TO 45~)**
d/t increase SV\*and HR.
43
What happens to **alveolar ventilation** during pregnancy?
Increase progesterone= increase alveolar ventilation: barely affects RR, but **increase tidal volume -\> + alveolar ventilation.**
44
What happens to **GI** during pregnancy?
* **Morning sickness** until 14-16 wks
* **Acid reflex**: d/t longer gastric emptying time and decrease in GE sphincter tone.
* **Increase water absorption and constipation:** d/t decrease colon movement
* **Need more _iron_, _protein_ and _folic acid_**
45
**PARTUTRITION: process of giving birth.**
## Footnote
**When does this occur and what is the status of our uterus while PG?**
1. Uterus is **quiet** while PG d/t **progesterone and relaxin.**
2. Birth occurs **38 weeks after fertilization** and **40 weeks after last pd.**
46
Obstetric definition of **labor**:
**_regular_, _rhythmic_, & _forceful_ contractions that occur to allow cervix to thin and dilate.**
47
Once labor is initiated (unknown how), it is sustained by a series of ____ feedback mechanisms
**positive**
48
Fetal station is **where the presenting part of the bby is in the pelvis.**
* Presenting part:
* Ischial spines:
* 0 station:
*
* **Presenting part**: part of the baby leading the way in the canal
* **Ischial spine**: bone points on moms pelvis and narrowest part of pelvis
* **0 station:** when bbys head is even with ischial spine -\> bby is "engaged"
49
If the presenting part lies above the ischial spines, the station is reported as a \_\_\_\_\_\_\_\_\_\_\_\_
**-1 to 5**
50
Toward the end of pregnancy, the **_uterus becomes progressively more excitable_**, until finally it develops such _strong rhythmical contractions_ that the baby is expelled
**_Two major categories of effects lead up to the intense contractions:_**
1. Progressive **hormone changes**
2. Progressive **mechanical changes**
51
* Toward the end of pregnancy, the uterus becomes progressively more excitable, until finally it develops such strong rhythmical contractions that the baby is expelled
* Two major categories of effects lead up to the **intense contractions: –**
* **Progressive hormone changes**
* Progressive mechanical changes
1. **Estrogen** increases *degree* of uterine contraction and *makes oxytocin receptors.*
* During the 7th month, estrogen continues to increase, whereas progesterone remains constant.
2. **Prostaglandin** increases during partution and initiate labor.
* Estrogen and oxytocin -\> + prostaglandin release -\> enhance contraction and motility of uterine smooth muscle -\> DELIVERY :)
* **_PG-F2a_** and **_PG-E2_** increase uterine motility, and have been used to _induce labor_
* Uterine stretch -\> + prostaglandin
__3. **Oxytocin**
**4. Relaxin**
**5. Fetal _pituitary_**
**6. Fetal _adrenals_**
**7. Fetal _plasma membranes_**
52
Toward the end of pregnancy, the uterus becomes progressively more excitable, until finally it develops such strong rhythmical contractions that the baby is expelled
Two major categories of effects lead up to the intense contractions: –
* **Progressive hormone changes**
* Progressive mechanical changes
**OXYTOCIN**
**\_\_\_\_\_\_\_ increases number of oxytocin receptors.**
**\_\_\_\_\_\_\_\_ increases oxytocin release.**
**-both of these will increase oxytocin response -\> increase \_\_\_\_\_**
Estrogen. The uterus actually remains insensitive to oxytocin until ∼20 weeks of gestation. by wk 36, 80x higher
Stretch of cervix (ferguson reflex) -\> increase oxytoncin release -\> stimulates contractions tha**t susstain labor.**
53
Whereas the uterus is sensitive to **oxytocin** only \_\_\_\_\_\_\_\_\_\_\_\_\_\_, it is susceptible to **prostaglandins** \_\_\_\_\_\_\_\_\_\_
**at the end of pregnancy**
**throughout pregnancy**
54
* Increased ___________ secretion does not initiate the rhythmic uterine contractions characteristic of the onset of labor
* – Only _________ are believed to have a key role in the initiation of labor
* – Once labor is initiated (stage 1), maternal oxytocin is released in bursts, & the frequency of these bursts _______ as labor progresses
**Increased oxytocin secretion** does not initiate the rhythmic uterine contractions characteristic of the onset of labor – **Only prostaglandins** are believed to have a key role in the initiation of labor – Once labor is initiated (stage 1), maternal oxytocin is released in bursts, & the frequency of these bursts **increases** as labor progresses
55
**Oxytocin** can bind to _________ cells and can stimulate ______ release, which does what
decidual cells
**PGF2**
In 2nd stage of labor, it can help the **bby come out by increasing prostaglandins.**
56
When the bby is expelled, what happens?
OT causes uterus to contract IMMEDIATELY, preventing blood flow and loss.
57
Fetal plasma oxytocin levels are _______ after vaginal delivery than after delivery by cesarean section, presumably because the \_\_\_\_\_\_
higher
**fergusion refle**x stimulated release of OT -\> crosses placenta -\> fetus
58
OT in 3 stages of labor
1. 1st stage (initiation) -\> maternal OT is relaased in bursts, freq increases as labor progresses
2. 2nd stage: OT binds to decidual cells -\> + PGF2 -\> help expel bb
3. 3rd stage: constrict BV to promote blood coagulation.
59
* **Relaxin**
* **Fetal pituitary**
* **Fetal adrenals**
* **Fetal placental membranes**
* **Relaxin** keeps uterus quiet in pregnancy; levels increase labor; soften/dilate cervix.
* Fetal pituitary secretes **_oxytocin_**
* Fetal adrenals secrete **cortisol**, a uterine stimulant
* Fetal placental membranes release **prostaglandins** in high concentration.
60
Toward the end of pregnancy, the uterus becomes progressively more excitable, until finally it develops such strong rhythmical contractions that the baby is expelled
Two major categories of effects lead up to the intense contractions: –
* Progressive hormone changes
* **Progressive mechanical changes**
1. bbies head stretches cirvix
2. Causes contraction
3. Pushes bby. down and stretches cirvix more
4. cycle repeats
**why twin are born 19 days early**
61
6. Describe the positive feedback mechanism associated with labor.
Stretching of the cervix by the fetal head _increases prostaglandin and oxytocin release,_ which maintains uterine contractions, which pushes the fetus forward.
**1. fetus head drops lower in uterus-\> stretches cervix -\>**
* **Uterine contractions -\> cervix stretch again -\> repeat**
* **Release of oxytoxin from PP**
* **-\> uterine contractions -\> cervic stretch again -\>repeat**
* **-\> prostaglandins from uterine wall -\> uterine constractions -\> repeat**
62
**Contractions during pregnancy, onset of labor & during labor**
* During pregnancy: **Braxton-Hick contractions-\>** weak and slow contractions
* -\> become strong last hours of pregnancy
* -\> start to stretch cervix and push bby out; now called **labor contractions**
63
* Uterine contractions stimulate ________ release, which itself increases the intensity of uterine contractions
* Uterine activity stretches the cervix, thus stimulating _______ release through the Ferguson reflex.
* Because ____ stimulates further uterine contractions, these contractions become self-perpetuating
prostaglandin
oxytocin
oxytocin
64
**Describe the pathophysiology of preeclampsia.**
**Characterized by HTN and signs of damage to another organ system - often renal.**
Other symptoms: proteinuria & edema.
MOA: _poor_ trophoblastic _invasion of spiral arteries_ in preeclampsia.
* This leads to decreased uterine placental blood flow.
* -\> placental ischemia.
* -\> release of placental factors (PG and NO among them).
* -\> renal pressure natriuresis and increased total peripheral resistance (TPR).
* **-\> HTN.**
65
The fundamental secretory unit of the breast is the \_\_\_\_\_\_\_.
**_alveolus_, arranged into *lobules* that drain milk into *ductules*.**
66
Describe the hormonal regulation of the mammary gland development
* **puberty vs.**
* **pregnancy**
**_Puberty_**: breast development depends on _estrogen_ and _progesterone_.
**_Pregnancy:_**
* Gradual increases in: PRL, hPL
* V High levels of: estrogen and progesterone
67
**Hormones affecting the breast are:**
1. _mammogenic_
2. _lactogenic_
3. _galactokinetic_
4. _galactopoietic_
1. **mammogenic**: cause proliferation of alveolar and duct cells
2. **lactogenic**: initiation of milk production by alveolar cells
3. **galactokinetic**: contraction of myoepithelial cells, & thus milk ejection), or
4. **galactopoietic**: (maintaining milk production after it has been established)
68
Epithelial cells in the **alveoli** secrete the components of milk by five major routes:
**1. Secretory pathway**
**2. Transcellular endocytosis and exocytosis. (IgA**
**3. Lipid pathway**
**4. Transcellular salt and water transport**
**5. Paracellular Pathway**
69
Epithelial cells in the alveoli secrete the components of milk by five major routes
## Footnote
**1. Secretory pathway**
2. Transcellular endocytosis and exocytosis. (IgA
3. Lipid pathway
4. Transcellular salt and water transport
5. Paracellular Pathway
1. Milk proteins lactalbumin and casein are made in the ER --\> golgi.
2. Alveolar cells add Ca2+ and Phosphate to the lumen of the Golgi.
3. Lactose synthetase in the golgi causes lactose synthesis.
4. Water enters by osmosis.
5. Proteins are exocytosed into the alveolar lumen.
70
Epithelial cells in the alveoli secrete the components of milk by five major routes
* 1. Secretory pathway
* **2. Transcellular endocytosis and exocytosis. (IgA**
* 3. Lipid pathway
* 4. Transcellular salt and water transport
* 5. Paracellular Pathway
1. Maternal immunoglobulins are taken up by endocytosis through the basolateral membrane.
2. They are then secreted into the lumen via exocytosis.
3. Infants GI system take up (mostly IgA) -\> immunity
71
Epithelial cells in the alveoli secrete the components of milk by five major routes
* 1. Secretory pathway
* 2. Transcellular endocytosis and exocytosis. (IgA)
* **3. Lipid pathway**
* 4. Transcellular salt and water transport
* 5. Paracellular Pathway
**FA from diet or fat stores (longer chain DA: \>16 carbons), which make up milk, are taken up are pushed into the lumen --\> vesicles.**
72
Epithelial cells in the alveoli secrete the components of milk by five major routes
* 1. Secretory pathway
* 2. Transcellular endocytosis and exocytosis. (IgA)
* 3. Lipid pathway
* **4. Transcellular salt and water transport**
* 5. Paracellular Pathway
Small electroltytes, salt and water is transported trancellulary from interstitial fluid -\> lumen of alveolus. Water follows osmotic gradient made by lactose.
73
Epithelial cells in the alveoli secrete the components of milk by five major routes
* 1. Secretory pathway
* 2. Transcellular endocytosis and exocytosis. (IgA)
* 3. Lipid pathway
* 4. Transcellular salt and water transport
* **5. Paracellular Pathway**
* Salt and water move into the lumen of the alveolus -\> through tight junctions.
* Cells, mainly leukocytes can squeeze between cells and NTR milk
74
10.Describe the hormonal changes associated with lactation (i.e. during **pregnancy** vs.
initiation of lactation).
Pregnancy
* AP. -\> **prolactin** -\> stimulates milk production early in pregnancy.
* BLOCKED: by estrogen and progesterone until they drop at parturition.
* **Human placental lactogen** is also lactogenic.
* At. end of pregnancy, breats fully developed, milk production is supressed except for small amount of **colostrum**.
75
what is colustrum?
**Colostrum** is a thin, yellowish milk-like substance secreted the first few days after birth; **contains a high concentration of immunoglobulins**
76
Describe the hormonal changes associated with lactation (i.e. during pregnancy vs.
**initiation of lactation).**
Initiation of lactation requires coordinated actions of seceral hormones.
1. **Prolactin↑**: mammogenic, lactogenic, galactopoietic
2. **Estrogen & Progesterone↓**
3. **Suckling** -\> Primary neural stimulus post- birth and most POWERFUL physiological stimulus for PRL release; inhibits DA
77
* Placental estrogens _______ PRL secretion during pregnancy –
* However, high estrogen & progesterone _____ onset of lactogenesis –
* Lactogenesis necessitates the _______ in estrogens & progesterone that accompanies parturition
**increase PRL**
**inhibit**
**abrupt fall**
78
\_\_\_\_\_\_ • Is the classic lactogenic hormone
**prolactin**
79
**Prolactin**
prolactin-\>
\_\_\_\_\_ release of GnRH -\> ____ in LH and FSH –
High levels of prolactin may lead to\_\_\_\_\_\_\_\_
Feedback also **decreases** release of GnRH with resulting **decreases** in LH and FSH – High levels of prolactin may lead to **lactational amenorrhea**
80
**Actions of PRL on the mammary glands include:**
* the promotion of **mammary growth** (**mammogenic** effect),
* the initiation of milk secretion (**lactogenic** effect), & the
* maintenance of milk production once it has been established (**galactopoietic** effect)
81
How does **oxytocin** enhance milk ejection
(**galactokinetic** effect)- contracts myoepithelial cells around. alveoli and ducts
+FB of sucking causes more OT to be made and released
82
11.Explain the effects of **suckling** on hormone release during lactation.
* 1. Sucking stimuli (or sight/sound of child) activates afferent neural pathway from breast -\> SC -\> hypothalamus
* 2. DA release inhibited -\> prolactin is released -\> milk production
* 3. SC stimulate production and release of **OT** from PP
* 4. SC neurons inhibit the arcuate & preoptic area of the hypothalamus -\> **- in GnRH production** -\> **- LH & FSH** -\> **inhibits the ovarian cycle**
