REPRODUCTION Flashcards

1
Q

What is the function of the testes?

A
  • To make sperm (mature spermatagonia) for spermatogenesis
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2
Q

What can cause infertility in men?

A
  • If a varicose vein occurs

- this will INTERRUPT the blood flow so venous blood can’t cool arterial blood coming into testis

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3
Q

Which two components is the testis made of?

A
  1. Seminiferous tubules
  2. Interstitial compartment (b/w seminiferous tubules (Leydig cells –> makes testosterone) –> contains blood vessels, lymphatics, and nerves
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4
Q

Which two structures are the seminiferous tubules and interstitial compartment (leydig cells) REGULATED by ? -

A
  • Pituitary and hypothalamus
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5
Q

What do leydig cells produce and which hormone are they regulated by?

A
  • Produce TESTOSTERONE and are regulated by LH

so decreased LH means decreased testosterone production

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6
Q

Why do smeiniferous tubules have a high amount of testosterone?

A
  • Because leydig cells are SO CLOSE to the tubules and testosterone is a steroid hormone so can easily diffuse in
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7
Q

In males, what hormone receptors do leydig and sertoli cells have respectivley?

A
  • LH (leydig) and FSH (sertoli) `
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8
Q

What hormone do Leydig cells and Sertoli cells produce respectively?

A
  • Testosterone (leydig) and Estrogen (MAINLY INHIBIN THOUGH) for Sertoli cells
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9
Q

What is the role of sertoli cells mainly? (male repro.)

A
  • They stimulate spermatogenesis
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10
Q

What does the inhibin negatively feedback on when produced by the sertoli cells in males?

A

-Feeds back negatively on the anterior pituitary to decrease FSH production

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11
Q

What does Testosterone feedback on in males?

A
  • LH
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12
Q

What are the androgenic actions of testosterone?

A
  • Initiation and maintenance of spermatogenesis, maintenance of secondary sex characteristics (from testosterone–> DHT (Dihydrotestosterone)
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13
Q

What are the anabolic actions of testosterone?

A
  • INCREASE in basal metaobolic rate
  • INCREASE in rate of protein synthesis
  • INCREASE in muscle mass
  • INCREASE in RBCs (erythropoesis)
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14
Q

What happens after puberty has hit in males?

A
  • testosterone STIMULATES spermatogenesis
  • INCREASES growth of reproductive ducts and glands
  • INCREASES the size of the penis
  • ENHANCES ability to maintain en erection
  • STIMULATES male secondary sex characteristics (not involved in reproduction)
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15
Q

Where does spermatogenesis occur?

A
  • In the seminiferous tubules of testis
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16
Q

Where do sertoli cells sit and what are 5 roles of it?

A
  • Sit in the basement membrane and cytoplasm surrounds developing germ cells
    1. Produce INHIBIN which feeds back to pituitary to DECREASE FSH secretion
    2. Paracrine activity within testes and acts on leydig cells
    3. Produce ABP (androgen binding protein)–> to allow for androgen rich environment
    4. Sertoli cells convert testosterone–> estradiol
    5. Important in blood brain barrier (form tight junctions)
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17
Q

What are the mechanisms of development of spermatazoa into sperm? (maturation)

A
  • Maturation occurs in epididimys

- Head of mature sperm CONDENSES –> so it only has nucleus and acrosomal cap that is formed from golgi

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18
Q

What do the acrosomal enzymes allow for?

A
  • Allow sperm to access ovum once in female reproductive tract
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19
Q

What are the 3 components of the sperm tail ?

A
  • Central skeleton of 11 microtubules–> axoneme similar to other cilia in other cells
  • Thin membrane covering axoneme
  • Collection of mictochondria SURROUNDING axoneme
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20
Q

How is testosterone secreted (in what form)?

A
  • Bound to ABP (androgen binding protein)
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21
Q

What is released in pulses every 90 mins to stimulate release of LH and FSH?

A
  • GnRH form hypothalamus
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22
Q

Which two hormones are required for spermatogenesis to occur?

A
  • FSH and HIGH TESTOSTERONE
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23
Q

What are examples of primary male infertility?

A
  • Failure WITHIN testes, seminiferous tubules, or leydig cells
    e. g. Klinefelters syndrome, and chryptochidism-failure of testes to descend)
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24
Q

What will a plasma test show for testosterone and LH + FSH levels?

A
  • LOW testosterone and HIGH LH and FSH
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25
Q

What is a secondary male infertility?

A
  • Failure of pituitary OR hypothalamus
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26
Q

What will plasma tests show for a secondary male infertility?

A
  • LOW gonadotrophins (lH and FSH) and LOW testosterone
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27
Q

What is the role of the female reproductive system?

A
  • To produce eggs and nurture and develop fetus
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28
Q

What do we mean when we say that female fertility is epsodic?

A
  • Female is NOT CONSTANTLY FERTILE (only fertile once a month after oocyte has been released)–> pattern of release of oestrogen and progesterone
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29
Q

What are the two functions of the ovaries?

A
  1. To produce OVA (oogenesis)

2. To secrete female sex hormones–> estrogen and progesterone

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30
Q

Which hormone is the period BEFORE ovulation dominated by?

A
  • Estrogen
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31
Q

Which hormone is the period AFTER ovulation dominated by?

A
  • Progesterone
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32
Q

Is the female reproductive system continuous like the male reproductive system?

A
  • NO
  • contains a gap between the ovary and fallopian tube –> some oocytes can’t make it and are lost in peritoneal cavity–> ECTOPIC pregnancy (can befetilised and implanted outside of tube)
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33
Q

Where is the ovary located?

A
  • In the pelvic region of the body inferior to the fallopian tubes and attached to the uterus via broad ligament
  • Has a number of follicles in stroma of connective tissue (cortex of ovary)
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34
Q

What is a primary follicle?

A
  • Has primary oocyte surrounded by SINGLE layer of connective tissue derived granulosa cells
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35
Q

What happens to oocytes NOT surrounded by granulosa cells?

A
  • They die by apoptosis
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36
Q

what is oogenesis?

A
  • Development of primordial germ cells to mature fertilisable oocytes
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37
Q

Oocytes are in a state of ________ and are reinitiated at ovulation and fininshed at fertilisation

A

-: Suspended meiotic division

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38
Q

What occurs in the process from primordial follcile –> Primary follicle?

A
  • Oocyte grows in size
  • More granulosa cells (but still only single layer)
  • Zona pellucida forms
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39
Q

What occurs in the process from primary follicle –> Preantral follicle?

A
  • Many more granulosa cells form

- Theca cell forms on outside (developed from connective tissue)

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40
Q

What occurs in the process from Primary (preantral) follicle–> Early antral Follicle?

A
  • Antrum forms –> contains secretory fluid of granulosa cells
  • theca cell INCREASES to MULTIPLE layers
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41
Q

What occurs in the process from Early Antral Follicle–> Graafian (mature) follicle?

A
  • ALL cell layers increase (more granulosa and theca cells)
  • Antrum layer
  • Oocyte moves to ONE POLE of follicle
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42
Q

Where (in general) do FSH and LH stimulate steoid synthesis in ?

A
  • In Antral follicles
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43
Q

In female reproduction, which cell type does FSH stimulate?

A
  • Granuloa cells
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44
Q

In female reproduciton, which cell type does LH stimulate?

A
  • Theca cells
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45
Q

What do Theca cells produce (female reproduction) ?

A
  • Androgens (Androstenedione–> testosterone)

- they are a substrate for estrogen production

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46
Q

What is the actions of the estrogens (oesdradiol) produced by the granulosa cell?

A
  • Further increase granulosa cell proliferation (positive feedback)
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47
Q

What occurs one week into the menstrual cycle?

A
  • ONE antral follicle will develop whilst others will undergo ATRESIA (degeneration)
48
Q

What kinds of receptors does the THECA cell have?

A
  • LH and Inhibin receptors
49
Q

What kinds of receptors does the granulosa cell have?

A
  • FSH and LH receptors
50
Q

What happens with an aromatase defficiency in females/ -

A
  • LESS estradiol and MORE testosterone build up (bc. can’t be converted to estradiol)
  • testosterone then escapes into the circulatioin (PCOS)
51
Q

what does not producing enough estradiol result in? (in terms of feedbacks)

A
  • You don’t get the switch from -ve–> +ve feedback THUS NO OVULATION
52
Q

What is leutinisation/what occurs during the process ?

A
  • Remaining cells (after oocyte in ovulation undergo this)
  • Collapsed follicle becomes corpus luteum–> membrane seaprating granulosa and theca cells breaks down and blood vessles invade
  • Luetinisation of theca and granulosa cells–> cells produce progesterone, inhibin and oxytocin
  • Hormones that convert progesterone to testosterone and estradiol DECREASE in activity
53
Q

If egg is not fertilised what happens?

A
  • Corpus luteum–> corpus albicans
54
Q

Which pathway will MOST follicles undergo and why?

A
  • Atresia
  • insufficient LH receptors or insufficient levels of LH or FSH
  • Follicle will end up degenerating
55
Q

What is NECESSARY for the secondary early antral folliclees to form from antral follicles?

A
  • FSH receptors

- So testosterone and estrogen can be made –> once the dominant follicle chosen

56
Q

What determines the dominant follicle?

A
  • One that makes the most estradiol
  • One that has the MOST LH receptors–> this follicle will then ovulate oocyte
  • After cell is ovulated, cells remaining make PROGESTERONE (corpus luteum)
57
Q

What does the corpus luteum secrete?

A
  • Progesterone
58
Q

What is the first 14 days of the menstrual cycle called?

A
  • Follicular phase
59
Q

What is the main estrogen present during the menstrual cycle?

A
  • Estradiol
60
Q

In the follicular phase of the cycle, which hormones are increasing? ***

A
  • Estrogen (estradiol)
  • testosterone
  • FSH + LH (less of increase in FSH)
61
Q

Which day does ovulation occur at of the cycle?

A
  • Approx day 13/14
62
Q

After ovulation, what are the hormone balances like in the luteal/secretory phase? *

A
  • Increase in progesterone
  • Estradiol and testosterone DECREASE
  • LH and FSH go back to normal
63
Q

What is the thickening of the endometrium driven by?

A
  • Estradiol
  • ## Day 14 onwards it peaks and plateus –> lasts during luteal phase and maintained from HIGH levels of PROGESTERONE
64
Q

What occurs to the endometrium thickness if the egg is not fertilised?

A
  • corpus luteum DEGENERATES–> progesterone decreases –> lining thins
65
Q

What drives ovulation?

A
  • Change in feedback–> estradiol +vley feeds back (instead of negative) at PRE-OVULATORY phase –> so increase in estradiol –> increase in LH then increase in estradiol again UNTIL OVULATION REACHED
66
Q

What happens once ovulation is reached in terms of postivie feedback?

A
  • It STOPS (return to neg feedback)
67
Q

What is the key mechanism of the ovulation of the dominant follicle?

A
  • Switch from negative –> positive feedback (only for short period of time) –> GnRH pulses (hypothalamus) cause the -ve –> + ve feedback
68
Q

Which two phases does the uterine cycle consist of?

A
  1. Follicular (proliferative) phase

2. Luteal (secretory) phase

69
Q

What occurs in the follicular (proliferative) phase of the uterine cycle?

A
  • Oestrogen DRIVES it (endothelial cell formation)
  • Proliferation of the glandular, stromal, and vascular (spiral) arteries and endothelial cells
  • THICKENING of mucosa
70
Q

What occurs in the luteal (secretory) phase of the uterine cycle?

A
  • Progesterone from corpus luteum maintains THICKNESS of cells and STIMULATES them to secrete—-> glycoproteins and nutrients to support fertilised egg –> becomes moist and soft for egg to become implanted in
71
Q

What is the key to maintaining a thick endometrium?-

A
  • Progesterone
72
Q

What casues bleeding from the menses?

A
  • When the corpus luteum sloths off–> spiral blod vessels SNAP (spasmoidic contractions and ichaemia)–> bleeding from spiral arteries
  • Endometrium slothed off with bleeding
73
Q

What happens to the GnRH pulses to switch the negative feedback from negative to positive up until ovulation?

A
  • The GnRH pulses become more FREQUENT
74
Q

What is the role of estrogens at puberty?

A
  • PROMOTE oogenesis
  • INCREASE growth of vagina, uterus, fallopian tube
  • Induce intital growth spurt BUT then close epiphyses of long bones
75
Q

What do progesterone and estrogen work together to do?

A
  • REGULATE the uterine cycle and changes in the cervical mucous
  • MAINTAIN pregnancy and SIMULATE breast growth
76
Q

What are the most common cause for no ovulation (infertility)?

A

PCOS (decreased oestrogen and increased testosterone)

  • More LH than FSH (increased LH: FSH ratio)
  • NO SWITCHING of GNRH pulses
  • HIGH androgens –> increased facial hair and androgens
77
Q

What does the binding of FSH to the FSH receptor on Granulosa cells lead to the production of initially?

A
  • Aromatase

- This converts testosterone into estrogen which is needed for ovulation

78
Q

What occurs in the fallopian tube disturbances to do with infertility?

A
  • BLOCKED fallopian tubes –> pelvic inflammatory disease and chlamydia OR endometriosis if scarring in tubes
79
Q

What occurs in uterine disturbances in infertility?

A
  • POLYPS in uterus–> overgrowth of endometrial lining (very thick ) –> miscarriage can happen as it restricts growth
  • FIBROIDS – >smooth muscle tumours (benign)
  • LUTEAL PHASE DEFFICIENCY–> Implantation disorder –> corpus luteum breaks down TOO early (won’t maintain pregnancy)
80
Q

What are the 6 steps to fertilisation?

A
  1. Sperm weave through granulosa cells
  2. Sperm bind to zona pellucida, causing increased calcium levels in sperm which leads to breakdown of membranes (acrosomal reaction)
  3. Acrosomal enzymes digest holes in the zona pellicuia
  4. An acrosomal process is formed at tip of sperm allowing it to bind to receptors on the egg
  5. Sperm and oocyte membranes fuse releasing sperm DNA into the egg
  6. Entry of sperm contents causes INCREASED calcium level in egg. This triggers the cortical reaction which destroys sperm receptors and hardens the zona pellucida which blocks polyspermy. twins are split embryos or two egg.
81
Q

What is the process of growth of the embryo in early stages (from fertilisation)?

A
  • Zygote–> morula–> (solid ball of blastomeres) –> Early blastocyst (hollow ball)–> Implanting blastocyst (trophoblast layer, inner cell mass, and blastocyst cavity
82
Q

To maximise the effects of fertilisation, when does intercourse occur?

A
  • A few days before or ON the day of ovulation (after ovulation oocyte can survive for 12-24 hours)
83
Q

How long can sperm survive in the reproductive tract for?

A
  • 4 days approx. (up to)
84
Q

What is the rough pathway of fertilisation?

A
  • Millions of sperm leak into the vagina–> ones that remain either get killed by vaginal acid or get trapped in the thick mucous
  • Ones that live and reach the ova must wait for capacitation to occur –> surface over acrosomal cap breaks down–> releases acrosomal enzymes that break down the zona pellucida—> breaks down and is able to access ova
85
Q

Which compartments does the sperm have to travel through to fertilise the egg?

A
  • Vagina–> cervix–> cervical mucous–> uterus–> up uterus–> right fallopian tube
86
Q

What is the process of ovulation to fertilisation?

A
  • In ovulation, the follicle ruptures and mature ovum is EXPELLED with surrounding CUMULUS cells into the FIMBRIA of fallopian tubes or oviduct
  • MOVEMENT of OVUM –> cilia lining oviducts SWEEP it along. Transport is dependent on presence of cilia and cumulus cells
  • Ovum and spermatazoa COME TOGETHER in the ampula of oviduct –> fertilisation occurs (only viable for 6-24hrs)
87
Q

Where do the ovum and spermatazoa come together?

A
  • In the ampulla of oviduct
88
Q

What do high progesterone levels lead to in fertilisation?

A

-Allow for decidualisation of endometrium (cellular changes in endometrium–> allow for implantation)

89
Q

What can an implantation failure be to do with?

A
  • Due to LACK of hCG (human chorionic gonadotropin)
  • Uterus scarring
  • Hormonal Imbalances (endometriosis, PCOS)
  • Non receptive endometrium (If endometrium hasn’t developed properly during secretory and follicular phase)
90
Q

What does a lack of hCG lead to?

A
  • Decrease in estrogen and progesterone
91
Q

What is an ectopic pregnancy?

A
  • Implantation OUTSIDE of uterus
  • IF IN fallopian tube–> tubal pregnancy
  • If in cervis (tubal pregnancy) –> Placenta previa–> problems in having space to develop placenta and delivery
92
Q

Which layer of blastocyst does placenta form from?

A
  • Trophoblast layer
93
Q

What is the function of the placenta?

A
  • Anchors fetus to uterine wall
  • Provides fetus with nutrients and removes wastes
  • DIRECTS maternal and homeostatic adjustments to meet changing fetal needs
  • Is like an endocrine organ –> secretes hormones
94
Q

What are the hormones that the placenta produces?

A
  • VERY early in pregnancy–> hCG

- hCG cells produced by trophoblast cells

95
Q

What is the action of hCH produced by the palcenta?

A
  • Prevents menstruation and PROLONGS the corpus luteum (prevents deterioration)
96
Q

What are the actions of progesterone DURING pregnancy?

A
  • Facilitates implantation
  • Maintains decidual lining of uterus
  • Relaxes smooth muscle (myometrium) -> suppressing endometrial contractions
  • Has peripheral effects on organs that have to adapt to pregnancy
97
Q

Are all 3 estrogens produced during pregnancy?

A
  • YES
98
Q

Which hormone is produced THE MOST by the placenta during prengancy?

A
  • hCG
99
Q

What do the estrogens do during pregnancy?

A
  • Stimulate utero-placental blood flow
  • Uterine growth
  • Breast development
100
Q

What does the placenta work with to produce estrogen and hCG?

A
  • the fetal adrenal gland
101
Q

Which steorid hormones does the maternal circulation provide to the placenta?

A
  • Cholesterol and progesterone and DHEA (in form of pregnenolone–> placenta converts pregnenolone to prgestereone)
102
Q

What is the placenta specific estrogen?

A
  • E3–> Estriol
103
Q

What are the protein hormones that the placenta produces?

A
  • hCG

- HPL (human placental lactogen)–> secreted from placenta

104
Q

What is the function of HPL?

A
  • Anti insulin properties
  • Stimualtes fat and carbohydrate absorption (similar to GH)
  • Proportional to placental mass
  • Stimulates mammary glands and energy to fetus
  • Stimulates insulin release by pancreas and increases plasma FAs
105
Q

What happens in terms of insulin in pregnancy?

A
  • blood glucose DECREASES, insulin INCREASES (placenta) and peripheral insulin resistance INCREASES (to ensure sufficient glucose for the fetus)
106
Q

What are the other peptide hormones are released from the placenta (3-4) and what do these all act to do?

A
  • PTH related peptide (INCREASES serum calcium)
  • Relaxin–> softens cervix ligaments and weakens pubic symphysis)
  • ACTH and CRH
  • ALL act to increase HR, BP, b.glucose, and stimulates partuition (timing and initiation of labour)
107
Q

Which 3 hormones reach increasing levels towards the end of pregnancy?

A
  • Placental CRH, ACTH and cortisol
108
Q

what does the cortisol secretion from the fetal adrenal cortex cause?

A
  • Acts on fetal lungs and increases surfactant production

- Gets lungs ready for breathing air

109
Q

What is the function of DHEA on placenta?

A
  • Causes placenta to convert DHEA to estrogen
  • Estrogen then has actions of increasing gap junctions in myometiral cells (contracting as unit)
  • Increase in uterine responsiveness to low levels of oxytocin (increases uterine contractions)
  • Increases in prostoglandin production–> cervical softening
110
Q

What are the maternal adaptations to pregnancy?

A
  • Driven by hormones secreted into the maternal circulation by placenta
111
Q

What are the cardiovascular changes that occur in pregnancy (maternal adaptations) ?

A
  • Increase in blood volume (hypervolemia) -via RAS and Cardiac Output
  • Decrease in TPR
  • Hypervolemia–> Nutrients to fetus, supports amniotic fluid production, supports enlarged uterus and hypertrophied vascular system
112
Q

What are the blood changes that occur in pregnancy (maternal adaptations) ?

A
  • Increased RBCs but these don’t offset the INCREASE in plasma volume so haemocrit reduced in pregnancy (anaemia)
113
Q

What are the osmolarity changes that occur in pregnancy (maternal adaptations) ?

A
  • DECREASE in plasma osmolarity

- From REDUCED setpoint of osmoreceptors BUT mechanisms for regulating osmolarity stay the same

114
Q

What are the renal changes that occur in pregnancy (maternal adaptations) ?

A
  • INCREASE in renal flow (70%) –> increased glomerular filtration rate
  • INCREASE in Na+ retention–> increase in blood volume and fluid retention
115
Q

What are the respiratory changes that occur in pregnancy (maternal adaptations) ?

A
  • INCREASE in ventilation (luteal phase of mentral cycle–> continues until baby is DELVIERED)
  • Metabolic demands of fetus increase so increase in O2 ocnsumption and CO2
  • Ventilation increases by 40% (high conc. of progesterone actions) –> increase in TIDAL volume –> decrease in pCO2 (respiratory alkalosis) –> compensated for by DECREASED HCO3-
  • DECREASE in RV (displacement and limited contraction of diaphragm)
116
Q

What kind of pressure circulation in plasma is there (high or low)?

A
  • Low pressure