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Block 11 > Week 1+2 > Flashcards

Week 1+2 Flashcards

1
Q

Histology of the Uterus

A

Perimetrium - simple squamous & areolar connective tissue.
Myometrium - 3 layers
1. Outer longitudinal
2. Circular (thickest)
3. Inner longitudinal
Endometrium - 2 layers
1. Inner: simple columnar epithelium (ciliated & secretory cells)
2. Thick lamina propria: stratum functionalis & stratum basalis.

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2
Q

Capacitation

A
  1. Hyperactivation - activation of whiplash tail for greater motility.
  2. Acrosome reaction - interacts with ZP2/3 on zona pellucida, causing destablilisation of acrosomal head, allowing it to fuse with oocyte.
  3. Acrosome contains ACROSIN + HYALURONIDASE.
  4. Acrosin digests through Zona pellucida.
  5. Hyaluronidase used to digest through corona radiata.

Sperm need to go through capacitation to attain fertilizing properties.

Acrosome - head of the sperm.
Hyaluronidase - breaks down hyaluronic acid in the corona radiata.
Acrosin - digest through zona pellucida

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3
Q

What phase are primary and secondary oocyte arrested in?

A

Primary = Prophase I (Meiosis I)
Secondary = Metaphase II (Meiosis II)

LH surge stimulates resumption of Meiosis I

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4
Q

How is the egg activated?

A

When sperm binds it deposits C-phospholipase gamma = enzyme that starts signalling cascade that leads to calcium oscillations = resumption of metaphase II.
Cyclin B (component of Maturation Promoting Factor (MPF) complex)is destroyed in response to increased calcium levels.

MPF destroyed = initiation of meiosis in secondary oocyte.

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5
Q

How is polyspermia prevented?

A

Cortical granules move from the inside to the outside of the egg as the egg is underoing maturation.
Cortical granules exocytose in response to calcium flunctuations - releasing compounds that degrade the ZP2/3 glycoproteins to stop sperm from binding.

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6
Q

What is produced once Meiosis II is complete?

A
  1. Two polar bodies.
  2. One haploid ovum containing:
    - female pronucleus
    - Male pronucleus
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7
Q

Abnormal fertilisation

A
  1. Polyspermic - 3pn
  2. Digynic - 3pn
  3. Parthneogenetic - 1pn

Parthneogenetic - 1 female pronucleus

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8
Q

How is zygote formed?

A

Male and female pronuclei decondense, expand, and replicate their DNA in preparation for mitosis.
Pronuclei migrate towards each other, their nuclear enelops disintergrate and genetic material intermingles.

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9
Q

Morulla

A

16-32 flatten cells.
Cells called blastomeres.

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10
Q

What forms after the Morulla?

A

Day 5.
Blastocyst forms - blastocoel cavity and blastomeres (Totipotent cells).
Blastocoel cavity - liquid filled cavity.

Day 7: Blastocyst still. Totipotent cells (blastomeres) differentiate
- Trophoblasts/trophoectoderm = epithelium
- Pluroblasts/Inner cell mass = embryonic stem cells

Surrounded by glycoprotein (zona pellucida)

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11
Q

Conceptus

A

Developing embryo

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12
Q

How is corpus luteum maintained?

A

Conceptus has synchitiotrophoblasts (makes hCG - binds LH receptors) & progesterone production.

Progesterone production by Luteal cells in corpus luteum.
hCG decreases after first trimester.

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13
Q

Conceptus indepence

A

Independent of ovarian hormone production by week 6.
C19 androgens from foetal adrenal cortex.
Placenta aromatizes ANDROGENS to OESTRAGENS

Progesterone from conceptus produced from CHOLESTEROL.

hCG no longer need once embryo synthesises its own steroids.

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14
Q

Chorion & Amnion & Yolk Sac

Embryonic origins

A

Trophoblast and Mesoderm.

Epiblast and Mesoderm.

Hypoblast and Mesoderm.

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15
Q

Formation of trilaminar disc

from pluriblast

A
  1. Pluriblast > Epiblast + hypoblast (mesoderm inbetween)
  2. Mesoderm surrounds epiblast and hypoblast.
  3. Epiblast and hypoblast form cavities
    i) Epiblast + meso = amniotic
    ii) hypo + meso = yolk
    iii) meso = coelom
  4. Proembryonic disc - Epi, Meso, Hypo
  5. Trilaminar disc forms - Ectoderm, Mesoderm, Endoderm.
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16
Q

Monozygotic vs Dizygotic

A

Mono = early embryo splitting (own chorion & amnion). Fused mono-chorionic, diamniotic (1 chorion & own amnion). Mono-chorionic, mono-amniotic (split occurs in ICM, 1 chorion, 1 amnion). Embryonic disc split (occurs in trilaminar disc(1 & 1)).

Dizygotic = 2 Oocytes ovulated and fertilized at the same time.

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17
Q

IVF process

A
  1. Ovarian hyperstimulation - give GnRH antagonist (Ganirelix) to downregulate GnRH receptors.
  2. Inhibition of FSH and LH release. Preventing release of AMH so multiple follicles can develop.
  3. Stop Ganirelix. Give rFSH to maintain follicles and progress to 2nd oocytes.
  4. Aspirate Oocyte via transvaginal ultra sound.
  5. Sperm and Oocyte co-incubated for 24hrs.
  6. Fertilized egg allowed to grow in medium for 48hrs.
  7. 2 embryos transferred to patient uterus via catheter.

If fertilized doesnt occur, can use Intracytoplasmic sperm injection (ICSI) to inject sperm directly into the Oocyte.

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18
Q

Sperm extraction methods

A

PESA - percutaneous epididymal sperm aspiration.
TESE - testicular sperm extraction.
TESA - testicular sperm aspiration.
MESA - microepididymal sperm aspiration.

azoospermia = no sperm

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19
Q

First trimeseter fetal development

A

Fertilization.
Implantation.
Initial development.
Placentation.

Mother experiences weight gain and nausea.

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20
Q

Second trimester fetal development

A

Nervous system.
Spine straightens.
Hair.
Ability to feel pain.
Proportion changes

Mother experiences, fundus rising, hypervolemia, cardiac remodelling, breast remodelling, placental growth.

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21
Q

Third trimester fetal development

A

Growth.
Fat deposition.
Brain growth.
Blood cells ( gamma chains replaced by beta chains).
Lung development.

Mother experiences Braxton-Hicks contractions (fake contractions), tired, restricted breathing, lactation.

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22
Q

Implantation process

A
  1. Blastocyst ZP and Glycocalyx is lost.
  2. Uterine epithelium produces LIF (Leukaemia Inhibitory Factor) to locally mediate implantation.
  3. Villous trophectoderm interdigitate (interlock) with villi on epithelium.
  4. Nuclei of epithelial cells of uterus move to basal pole of cell.
  5. Trophoblast cells invade uterine epithelium.
  6. Primary decidua is locally destroyed by trophoblast with proteases.
  7. Endometrial epithelium seals over the blastocyst in endometrial wall.
  8. Trophoblasts turn into Synctial trophoblasts and form Syncytium (one cytoplasmic mass w/ many nuclei) around inner layer of trophoblasts > turns into Cytotrophoblasts.
  9. Fragments of maternal capillaries engulfed by Syncytium.
  10. Trophoblastic lacunae fill with materal blood and are precursors of intervillos spaces of the placenta.
  11. Maternal capillaries expand to form sinusoids that anastomose with the trophoblastic lacunae.
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23
Q

What is Decidualisation?

A

Process that results in significant changes to cells of the endometrium in preparation for pregnancy and during pregnancy.

Decidua basalis (primary decidua) - between placenta and myometrium.
Decidua capsularis - encapsulates chorion.
Decidua parietalis - lines myometrium where there is no basalis.
Deciduous spiral arteries.

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24
Q

Endometrial blood supply remodelling to form Placenta

A
  1. Stem villi form from Syncytiotrophoblast and extend into the intervillous space within syncytium.
  2. Small villi form from the stem villus to create a network of terminal villi (site of gas exchange).
  3. Villi developed in 3 stages:
    i) Primary - composed of syncytium
    ii) Secondary - mesoderm invades villous core
    iii) Tertiary - Blood vessels developed from mesoderm
  4. Spiral arteries remodelled by replacement of smooth muscle and endothelium w/ trophoblast todrop pressure and increase volume (allows blood to pool) - deciduous spiral arteries.
  5. Deciduous spiral arteries expand to form sinusoids that enter intervillous spaces (Lacunae) & bathe foetal villi in oxygenated blood.
  6. Deoxygenated blood flows back to mother through endometrial veins.
  7. Umbilical vein carries blood away from the villi.
  8. Umbilical vessels from fetus enter Cytotrophoblast layer to form Chorionic vessels which supply villi.

placenta formed by week 12.

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25
Q

Fetal Lobule

A

Intervillous space (lacunae) supplied by a villus (many terminating branches), deciduous spiral arteries, and endometrial veins.

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26
Q

Villi development in placenta

A
  1. Primary stem villi formed from Synctiotrophoblasts - solid core.
  2. Mesoderm invades core to form secondary villi.
  3. Mesoderm develops to form blood vessels & connective tissue - tertiary villi.
  4. Tertiary villi carry on developing:
    a) Mesenchymal villi - tertiary villi lengthen.
    b) Immature intermediate tertiary villi - tertiary villi reach maxium lengths.
    c) Mature intermediate tertiay villi - produce small nodule like secondary branches - Terminal villi
  5. Terminal villi formed - final structure of the villus tree.
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27
Q

Endocrine function of the placenta

A

hCG - maintains corpus luteum until Synctiotrophoblast are mature enough to produce enough progesterone to maintain the uterine lining.
Oestrogen - Conceptus adrenal cortex synthesis androgens which are converted to estrogens via androgen aromatase.
Progesterone.
Somatomammotropin.

Estrogens role: proliferative effect on mother, relax pelvic ligaments and increase elasticity of pubic symphysis.
Progesterone role: causes decidualisation, increases uterine secretions, reduces uterine contractions.

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28
Q

How does progesterone & estrogen cause hypervolemia?

A

Progesterone: Vasodilator, increases aldosterone, increases thirst
Estrogen: increased angiogenesis, vasodilator, increases production of angiotensin II by liver, increases aldosterone

Blood volume increased by 45%.
Corpus luteum regress in 2 trimester.

29
Q

Chadswick sign

A

Blue discolouration of cervix, vagina, and labia whilst pregnant due to increased blood flow.

30
Q

Changes in materal heart

A

Increase in size by 12%.
HR increased by 20%.
SV increased by 20%.

Increased due to proliferation and increased venous return.

Estrogens reduce Endothelin-1 = increases venous distensibility

31
Q

Respiratory changes during pregnancy

A

Rib cage displaced upwards.
Thoracic breathing.
Responsiveness to pCO2 increased by action of progesterone (increased tidal volume).
Peripheral chemoreceptor sensitivity is lowered so that high pO2 does not reduce RR.

Reduced total capcity - diaphragm elevation
Increased tidal volume - increases sensitivity to pCO2
Reduced residual volume - diaphragm elevation

32
Q

Changes in the upper and lower urinary tract

A

Upper
Kidneys enlarge.
- increased blood flow > increased excretion
- Increased reabsorption
Ureters displaced and enlarged.
Lower
Decreased bladder tone - urinary reflux = bladder stasis.
Urine rich in glucose and AA > increased risk of UTI.

33
Q

Breast changes during pregnancy

A

Stroma increases in bulk.
Lobules and alveoli increase in size.
Lactiferous ducts expand and branch.

Progesterone = stimulate growth of alveoli and lobules
Estrogen = stimulate growth of lactiferous
Human placental lactogen (HPL) = breast, nipple, areola enlargement

34
Q

What is Relaxin?

A

Secreted by placenta.
Cause cervix to dilate & loosens pelvic ligaments.

Secreted in T3, near birth

35
Q

What is labour?

A

Fetus is expelled outside of the uterus.
Forces of release > Forces of retention

36
Q

Forces of retention (6)

A

Progesterone - reduces contractibility of uterine muscles.
Cervix - does not soften until end of T3.
Hypervolemia - supresses oxytocin and vasopressin release from posterior pituitary.
Adrenaline - acts like progesterone.
Relaxin - reduces contractibility of uterine muscle.
CRH - inhibits release of prostaglandins.

CRH = corticotropin releasing hormone (Stress hormone)

37
Q

Forces of release (7)

A

Estrogen - relax pelvic ligaments and increases elasticity of pubic symphysis.
Oxytocin - increases contractibility of uterine muscles.
Vasopresin - increases contractibility of uterine muscles.
Cortisol - inhibits action of progesterone.
Prostaglandins - increase sensitivity of uterine muscle to oxytocin.
Uterine distention - maximal distention = contraction.
CRH - towards end of term it increases contractibility of uterine muscle.

38
Q

3 P’s

A

Passage.
Power.
Passenger.

39
Q

4 types of Pelvis

A
  1. Gynecoid: wide pubic arch (best)
    - Inlet = wider transverse diameter than AP
    - outlet = wider AP than transverse
  2. Android
    - Narrow pubic arch
    - Prominent ischial spines
  3. Anthropoid
    - Narrow pubic arch
    - Wider AP diameter than transverse
    - fetus engages in occipit-posterior position rather than occipit-anterior
  4. Platypelloid
    - wide pubic arch
    - wider transverse than AP
40
Q

Pelvic floor muscles

A

Coccygeus
Levator ani
- Puborectalis
- Pubococcygeus
- Illiococcygeus

41
Q

4 characteristics of uterus for delivery

A

Tone.
Contractility - start at fundus and work down.
Fundal dominance.
Rhythmicity.

42
Q

5 ways the babys head can be flexed

A
  1. Suboccipito-bregmatic - head flexed completely
  2. Suboccipito-frontal - head not fully flex = not ideal
  3. Occipito-frontal
  4. Mentovertical - head not fully extended = c section
  5. Submento-bregmatic - head completely extended

small diameter = subocciputo bregmatic
largest diameter = mentovertical

43
Q

Fontanels

A

Two major soft spots on infant head.
Fetal skull is squashed in labour, bones overlap.

44
Q

Cardinal movements

A
  1. Engagment
  2. Descent
  3. Flexion
  4. Internal rotation
  5. Extension
  6. External rotation
  7. Expulsion
45
Q

Stages of labour

A

Latent
- Onsent of contractions
- 3-4cm dilations
First stage
- Regular contractions
- cervix fully effaced
- reaches 10cm dilation
Second stage
- Passive: no pushing
- Active: Maternal pushing
- Delivery of baby
Third stage
- Delivery of placenta and membranes
- haemostasis

46
Q

How to induce labour

A
  • Oxytocin (Pitocin)
  • Prostaglandin E - if cervix is closed
  • Amniotomy - rupture membranes if cervix is open
  • Membrane sweep - stretch cervix - irritates and causes prostaglandin release
  • Natural stimulation - emptying bowels and intercourse (prostaglandins in semen)
47
Q

Physiology of child birth

A
  1. Progesterone levels diminish slowly – uterine contractions no longer inhibited
  2. Placenta secretes more CRH, which stimulates ACTH secretion from AP
  3. ACTH stimulates foetal adrenal gland to secrete Cortisol (blocks action of progesterone) and DHEA (Dehydroepiandrosterone) which is converted by the placenta to Oestrogen
  4. High levels of Oestrogen cause:
    a. Pelvic ligaments to relax and Increase in elasticity of pubic symphysis
    b. Increase in number of Oxytocin receptors on uterine muscle fibres
    c.Uterine muscles to form gap junctions between cells
    d. Release of prostaglandins by placenta
  5. Oxytocin release by posterior pituitary causes uterine contractions
  6. Relaxin release by placenta increases flexibility of pubic symphysis and dilates the cervix
  7. Prostaglandins induce production of enzymes that digest collagen fibres in cervix = softens
  8. Contraction of Uterine myometrium forces baby into cervix, distending it, stretch receptors in cervix send nerve impulses to Neurosecretory cells in hypothalamus causing increased release of Oxytocin – Stimulates further myometrium contraction – Positive feedback
48
Q

Fetal stress during labour

A

Caused by intermittent hypoxia due to compression of umbilical cord and placenta during contractions.
Fetal adrenal medullae secrete very high levels of epinephrine + norepinephrine that:
- clears lungs and alters their physiology ready or breathing air
- Mobilises nutrients for cellular metabolism
- Promotes increase of blood flow to brain and heart

49
Q

What happens after labour?

A

Lotchi: uterine discharge after birth, blood & serous fluid
Puerperioum - female reproductive organs back to pre-pregnant state. Reduction of uterus size. Occurs 6 weeks postpartum.

50
Q

How is fetal wellbeing monitored?

A

Intermittent auscultation.
CTG - CardioTopoGraph
i) ultrasound of fetal heart
ii) ultrasound of uterus (detects pressure waves > contractions)

51
Q

Hormones for mammary growth

A

Anterior Pituitary:
- Prolactin
- LH
Placenta:
- Human Placental Lactogen

Estrogen
Progesterone

52
Q

Mammogenesis in fetus

A
  1. Milk lines from axilla to groin of glandular epithelial tissue.
  2. Milk hills - Thickening and inward growth into chest wall.
  3. Differentiation - smooth muscle cells of nipple and areola.
    a) Epithelial cells form mammary buds which elongate to form ducts and alveoli
  4. Canalization of branched epithelial tissue - development of ductal system.
  5. Lobular-alveolar structurs develop.
  6. Ducts open into area that will become the nipple.
  7. Nipple and areolar develop and become pigmented.
53
Q

Breast changes from infancy to puberty

A

Birth:
Breast tissue confined to nipple area.
Childhood:
Mammary gland undergo limited growth.
Puberty:
Branching of ductules to form more alveoli.
Fat deposition creates shape and size of breast.

Development due to estrogen and HGH.

54
Q

Role of hormones in mammogenesis

A
  1. Estrogen: Stimulates ductual system proliferation and differentiation - ducts lengthen and branch out causing the breast to get bigger.
  2. Progesterone: Lobes, lobules, alveoli grow.
  3. Prolactin: Nipple growth. Complete lobular-alveoli development.
  4. ACTH + HGH: Combine with prolactin and progesterone to promote mammary growth.
55
Q

Tail of Spence
&
Tubercles of Montgomery

A

ToS: Tissue extending from breast towards shoulder/axilla

ToM: Pores on surface of areola - sebaceous gland.

56
Q

Rib level of Breast

A

2 to 6

57
Q

Internal structure of breast

A

Alveolus/Acinus > Lactiferous duct > intralobular terminal duct > Lobule > Extralobular terminal duct > Lobe > Lactiferous duct > Lactiferous sinus > Nipple opening

Alveolus lined with lactocytes surrounded by myoepithelial cells.

Arterial supply to lobules: Internal mammary & Lateral thoracic
Venous drainage: Internal and external mammary & Axillary
Lymph: Central and Deep axillary nodes

58
Q

Nerve supply of breast

A

2-6th intercostal nerves.
Mainly 4,5,6.

59
Q

Development of breast during pregnancy

A
  1. 6-8weeks:
    Increased blood supply.
  2. 12 weeks:
    Pigmentation of nipple and areola.
    Areola englarges.
    Nipples pronounced.
    Sebaceous glands secrete oil.
  3. 16 weeks:
    Colostrum production.
60
Q

Lactogenesis

A

3 phases.
i) 16 weeks gestation, colostrum production.
ii) Copious milk secretion following birth lasting until 96 hours post partum.
iii) Maintaince of milk supply via autocrine control.

61
Q

Lactogensis I

A
  1. Alveoli expanded through accumulation of colostrum due to prolactin in 2nd trimester.
  2. Alveolar epithelial cells differentiate into Lactocytes.
  3. Fat droplets accumulate in Lactocytes.
  4. High plasma concentration of lactose and lactalbumin.
  5. Milk droplets cross cell membrane into lumen of alveoli.
  6. High levels of estrogen/progesterone inhibit milk secretion in late pregnancy via inhibiting Prolactin action.

mid pregnnacy - 48 hours postpartum

62
Q

Lactogenesis II

A
  1. Closure of tight junctions between lactocytes prevents passage of substances between them.
  2. Onset of copious milk secretions.
  3. Sodium and protein levels of milk fall.
  4. Lactose and milk lipid levels rise.

day 3 - 8 postpartum.
Triggered by third stage of labour.
Lactation moves from endocrine to autocrine.

63
Q

Lactogenesis III

A

Sustained milk secretion.
Autocrine control.

64
Q

Theories of milk production

A

Prolactin receptor theory.
Feedback inhibitor of Lacation (FIL).

65
Q

Prolactin Receptor Theory

A

Prolactin receptors in wall of lactocytes distort when breast are full.
Prolactin detaches.
Reduction in milk production.

Frequent milk removal in the early weeks will increase receptor sites.

66
Q

Feedback Inhibitor of Lactation (FIL)

A

FIL - small whey like protein in brest milk
FIL slow milk synthesis when breast are full.

67
Q

Milk Let Down reflex

A

Suckling triggers oxytocin & prolactin to be released into circulation. Prolactin makes milk, Oxytocin causes myoepithelial cells to contract (secretion).

68
Q

Mastitis

A

inflammation of mammary gland.
Non-infective - 70%
Infective - 30%
Symptoms: Pyrexia, Unilateral, Clear demarcation, sudden onset (+ rigors in infective)
Treatment: Pencillinase resistant penicillins, cephalosporins, warm compress.

infective = staph aureus, sometimes strept or ecoli.

69
Q

Inhibit B

A

Secreted by Sertoli cells (men) & granulosa cells (female).
Inhibits secretion/synthesis of FSH from pituitary.

Block 11 (4 decks)

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