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PHYSIOLOGY 2 > REPRODUCTION > Flashcards

REPRODUCTION Flashcards

1
Q

Late luteal early follicular stage

Menstrual cycle

A

Low progesterone and high FSH

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2
Q

Mid follicular stage

Menstrual cycle

A

High Oestrogen = negative feedback

Low FSH

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3
Q

Mid cycle stage

Menstrual cycle

A

Oestrogen = positive feedback

Increase LH

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4
Q

Mid luteal stage

Menstrual cycle

A

Increase progesterone = negative feedback

Decrease LH & FSH

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5
Q

Describe the steps for follicle selection/dominant follicle

A
  1. high FSH - recruit antral follicles that are at the right stage to continue growth.
  2. Oestradiol levels increase and FSH levels fall
  3. Follicle that survives the decline of FSH becomes the dominant follicle
  4. As FSH fall, LH increases - dominant follicle requires LHR on GCs
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6
Q

Steps of ovulation

A

Occurs with release of cumulus oocyte complex

  1. Oocyte with cumulus extruded from ovary
  2. Follicular fluid pours into Pouch of Douglas
  3. Egg ‘collected’ by fimbria of fallopian tube
  4. Egg progresses down tube by peristalsis and action of cilia
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7
Q

Describe the structure of the testes

A

Basement membrane - primary germ cells or spermatogonia
Walls of tubule made of sertoli cells - tight junctions between = adluminal compartments.
Spaces between tubules are filled with blood and lymphatic vessels, leydig cells and interstitial fluid

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8
Q

Sperm stages during spermatogenesis

A 
Spermatogonia 
Primary spermatocytes 
Secondary spermatocytes 
Spermatids  
Spermatozoa
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9
Q

Capacitation

A

Partly achieved by removing the sperm from seminal fluid. Uterine or tubal fluid may contain factors which promote capacitation

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10
Q

Acrosome reaction

A

Occurs in contact with zona cumulus complex

Acrosomal membrane on the sperm head fuses releasing enzymes that cut through the complex

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11
Q

Acrosin

A

Bound to the inner acrosomal membrane - digests the zona pellucida so the sperm can enter

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12
Q

What happens in endometrial proliferative phase

A

Stimulated by oestrogen
Stromal cell division, ciliated surface. Glands expand, increase vascularity
When endometrium >4mm induction of progesterone receptors and small muscular contractions of myometrium

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13
Q

What happens in endometrial secretory phase

A

2-3 days after ovulation, gradual rise in progesterone causes reduction in cell division.
Oedema, increase vascular permeability, arterioles contract
Myometrial cells enlarge and movement suppressed

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14
Q

What happens in menstruation

A

Prostaglandin release cause constriction of spiral arteries. Hypoxia lead to necrosis.
Vessels dilate and bleeding ensues.
Proteolytic enzymes from dying tissue.

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15
Q

Changes in cells lining uterine tubes

A

Epithelial cells - high numbers of oestrogen receptors and undergo differentiation
Cilia beat and secretory cells are active along with muscle layer contractions
After a few days exposure to progesterone the oestrogen receptors are suppressed.

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16
Q

What is the ectocervix covered with

A

Non-keratinised stratified squamous epithelium - resembling the squamous epithelium lining the vagina

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17
Q

Cervix follicular phase

A

Oestrogen in follicular phase - change in vascularity of cervix and oedema
Change in mucous

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18
Q

Cervix luteal phase

A

Progesterone cause reduced secretion and viscous mucus

Glycoproteins form mesh like structure - acts as a barrier

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19
Q

Cardiovascular risks of COCP

A

HBP
Clotting disorders
Migraines - cannot have COCP due to concerns of stroke

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20
Q

GI risks of COCP

A

Insulin resistance
Weight gain
Crohns disease

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21
Q

Hepatic risks of COCP

A

Hormone metabolisms
congenital nonhemolytic jaundice
gall stones

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22
Q

What does IUCD do

A

Copper IUCD inserted into the uterus.
Destroy spermatoza
Prevent implantation - inflammatory reaction and prostaglandin secretion as well as mechanical effect

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23
Q

Risks of IUCD

A

Miscarriage if left in situ if pregnant
Ectopic
May be expelled if incorrectly inserted
Uterus may be perforated - need to know orientation of the uterus before insertion

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24
Q

Contraindications of IUCD

A

Current pelvic inflammatory disease
Suspected or known pregnancy
Unexplained vaginal bleeding
Abnormalities of the uterine cavity

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25
Q

Changes in glucose in 1st trimester

A

Pancreatic beta cells increase in number - plasma insulin increases, fasting serum glucose decrease

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26
Q

Changes in glucose in 2nd trimester

A

hPL cause insulin resistance - less glucose in stores = increased availability in serum glucose (more crosses placenta)

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27
Q

Changes in CVS in pregnancy

A

Increase CO

Increased HR and SV

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28
Q

Changes in vessels in pregnancy

A

Increased CO and vasodilation by steroids = reduced peripheral resistance
Increased flow to uterus, placenta, muscle, kidney and skin

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29
Q

Stages of implantation

A
  1. Apposition
  2. Attachment
  3. Invasion
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30
Q

Day 7-8 in implantation time line

A

Blastocyst attach to the surface of decidua basalis.

Trophoblast cells assemble to form SYNCYTIOTROPHOBLAST to facilitate invasion of decidua basalis

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31
Q

Day 9-11 in implantation time line

A

Syncytiotrophoblast further invades the decidua basalis and by day 11 it is almost buried in the decidua

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32
Q

Day 12 in implantation time line

A

Decidual reaction occurs - high levels of progesterone result in enlargement and coating of the decidual cells in glycogen and lipid rich fluid.
Fluid is taken up by syncytiotrophoblast and help sustain blastocyst before placenta is formed

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33
Q

Day 14 in implantation time line

A

Primary villi form all round blastocyst
Lacunae form
Blood vessels merge with the lacunae - maternal arteries and veins grow into decidua basalis
Blood filled lacunae merge into single pool of blood = junctional zone

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34
Q

How are primary villi formed

A

Cells of syncytiotrophoblast protrude to form tree like structures

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35
Q

How are lacunae formed

A

Decidual cells between primary villi begin to clear out, leaving behind spaces

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36
Q

What is the junctional zone

A

Blood filled with lacunae merge into single large pool of blood connected to multiple arteries and veins

37
Q

Day 17 in implantation/placenta time line

A

Foetal mesoderm cells start to form blood vessels within the villi – a basic network of arteries, veins, and capillaries. Capillaries connect with blood vessels in the umbilical cord
Villi grow and develop into chorionic frondosum.
At this point, endothelial cell wall and syncytiotrophoblast (villi) lining separate maternal and foetal RBCs

38
Q

4th and 5th month of placenta timeline

A

Decidual septa form as they divide placenta into 15-20 regions = COTYLEDONS
Maternal spiral arteries supply blood to each cotyledon, facilitates maternal foetal exchange

39
Q

Pre-eclampsia

A

Result in placental insufficiency – inadequate maternal blood flow to the placenta during pregnancy
Causes new onset maternal hypertension and proteinuria
Symptoms range from mild to life threatening
Characterised by the narrowing of maternal spiral arteries supplying blood to the placenta

40
Q

Risk factors of pre-eclampsia

A

1st pregnancy
Hypertension, diabetes, obesity
Hypertension - decreased blood flow in kidney and lead to proteinuria
Pre-eclampsia + seizures = eclampsia

41
Q

Cause of Placenta abruption

A

Degradation of maternal arteries supplying blood to the placenta. Degenerated vessels rupture causing haemorrhage and separation of the placenta

42
Q

Complications - maternal of placenta abruption

A

Hypovolemic shock
Sheehan syndrome
Renal failure
Disseminated intravascular coagulation (from release of thromboplastin)

43
Q

Complications - foteal of placenta abruption

A

Intrauterine hypoxia and asphyxia

Premature birth

44
Q

Placenta previa

A

Placenta implants in lower uterus, fully or partially covering the internal cervical os
Associated with increased chances of pre-term birth and foetal hypoxia

45
Q

Risk factors of placenta previa

A 
Previous caesarean delivery
Previous uterine/endometrial surgery
Uterine fibroids
Previous placenta previa
Smoking and recreational drug use
46
Q

Hormonal changes in pregnancy

A

Low ratio of oestrogen: progesterone to supress maturation of other follicles in the ovary
Placenta synthesised oestrogens from foetal androgens from foetal adrenal cortex
Placenta synthesised progesterone from maternal cholesterol

47
Q

Spermatogonia

A

Germ cell on basement membrane, capable of mitotic or meiotic division into spermatocytes or more spermatogonia by mitosis. They are diploid

48
Q

Primary spermatocytes

A

Move into adluminal compartment and duplicate their DNA into sister chromatids which exchange genetic material before entering meiosis I. 46XY diploid

49
Q

Secondary spermatocytes

A

Have undergone meiosis I to give 23X + 23Y haploid number of chromosomes arranged as sister chromatids

50
Q

Spermatids

A

Meiosis II occurs to give 4 haploid spermatids. Round spermatid to elongated spermatid differentiation

51
Q

Spermatoza

A

Mature sperm extruded into the lumen

52
Q

Sexual determination

A

Genetically controlled process dependent on the switch on the Y chromosome
Chromosomal determination of male or female

53
Q

Sexual differentiation

A

Process by which internal and external genitalia develop as male or female

54
Q

Primordial germ cells become

A

Sperm or oocytes

55
Q

Primitive sex cords become

A

Sertoli cells or granulosa cells

56
Q

Mesonephric cells become

A

Leydig cells or theca cells

57
Q

Gonadal dysgenesis - AIS

A

Testosterone is made but has no effect

Testis form and make AMH - regression of Mullerian ducts

58
Q

Complete AIS

A

Appear female at birth but is XY - undescended testes

Primary amenorrhoea and lack of body hair

59
Q

5 alpha reductase deficiency

A

Testosterone made but not DHT
Testes form and make AMH - Wolffian ducts develop
External structures do not develop
AUTOSOMAL RECESSIVE

60
Q

Turner syndrome

A

Females missing X chromosome

Uterus and tubes are present but small, other defects in growth and development

61
Q

Congenital adrenal hyperplasia (CAH)

A

No SRY, No testes, No AMH
Masculinised external genitalia, but androgen levels not high enough to save Wolffian ducts
Possibility of ‘salt wasting’ due to lack of aldosterone

62
Q

Pathway block leading to CAH

A

Failure to synthesise cortisol - (by 21 hydroxylase)

No negative feedback so CRH will stimulate pituitary to release ACTH

63
Q

Regulation of uterus by neurotransmitter

A

Sympathetic innervation
Expression of alpha and beta adrenoreceptors
alpha adrenoreceptor agonist = contraction
beta adrenoreceptor = relaxation

64
Q

Regulation of uterus by sex hormones

A

Progesterone inhibit contraction

Oestrogen increases contraction

65
Q

Hormones in a non pregnant uterus

A

Weak contractions

Strong contractions during menstruation - decrease progesterone, increase prostaglandin

66
Q

Hormones in pregnant uterus

A

Weak and uncoordinated contraction - high progesterone

Strong and coordinated contraction at parturition - high oestrogen

67
Q

Oestrogen/progesterone ratio during parturition

A

Increases
Oestrogen increases while progesterone decreases gap junction expression in myometrium
Oestrogen/progesterone also found in ICC

68
Q

Regulation by prostaglandins

A

Myo- and endo-metrium synthesise PGE2 and PGF2α – promoted by oestrogens
Both prostaglandins induce myometrial contraction
Role in dysmenorrhoea (severe menstrual pain), menorrhagia (severe menstrual blood loss), pain after parturition - NSAIDs are effective – decreased contraction and pain
Act together to:
Coordinate increased frequency/force of contractions
Increase gap junctions
Soften cervix

69
Q

Prostaglandin analogues

A

dinoprostone (PGE2)
Carboprost (PGF2α)
Misoprostol (PGE1)

70
Q

Uses of prostaglandin

A

Induction of labour - before term
Postpartum bleeding
Softening of cervix

71
Q

Concerns of prostaglandins

A

Dinoprostone can cause systemic vasodilation
Potential for CVS collapse
PGs - hypertonus and foetal distress

72
Q

What is oxytocin

A

Non-peptide hormone synthesised in hypothalamus and released from posterior pituitary gland
Effective at term

73
Q

Regulation by oxytocin

A

Oestrogen released after parturition produce - increase oxytocin release, oxytocin receptors and increase gap junctions.
Oxytocin also synthesises prostaglandins

74
Q

Pharmacological actions of sythetic versions of oxytocin

A

Low conc. of oxytocin analogue – increase frequency and force of contractions.
High concentrations cause hypertonus – may cause foetal distress

75
Q

Synthetic versions of oxytocin

A

Syntocinon and pitocin

76
Q

Uses of synthetic versions of oxytocin

A

Induction of labour at term – does not soften cervix
Treat/prevent post-partum haemorrhage
Syntometrine – oxytocin (rapid)/ergot (prolonged) combination

77
Q

Action of ergot

A

Powerful and prolonged uterine contractions - but only when myometrium is relaxed

78
Q

Mechanism of ergot

A

Stimulate alpha adrenoreceptors and 5HT receptors

79
Q

Uses of ergot

A

Post partum bleeding - not induction

80
Q

Myometrial relaxants

A

May be used in premature birth - delay delivery by 48hrs

81
Q

Beta adrenoreceptor stimulants

A

Salbutamol
Relax uterine contractions - direct action to myometrium
Used to reduce strength of contraction in premature labour
May occur as a side effect of drugs used in asthma

82
Q

Ca2+ channel antagonist

A

Nifedipine
Used in hypertension
Or mg sulfate

83
Q

Oxytocin receptor antagonists

A

Retosiban

84
Q

COX inhibitors

A

NSAIDs

85
Q

What to use for induction of labour

A

Oxytocin

86
Q

What to use for Induction labour/termination in early term

A

Prostaglandins

87
Q

What to use for post partum bleeding

A

Prostaglandins
Oxytocin
Ergots

88
Q

What to use to prevent premature birth

A

Beta 2 adrenoreceptor agonists
Ca2+ channel blockers, Mg sulphate
Oxytocin inhibitors

PHYSIOLOGY 2 (5 decks)

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