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PHYSIOLOGY 2 > REPRODUCTION > Flashcards

REPRODUCTION Flashcards

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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
Changes in glucose in 1st trimester
Pancreatic beta cells increase in number - plasma insulin increases, fasting serum glucose decrease
26
Changes in glucose in 2nd trimester
hPL cause insulin resistance - less glucose in stores = increased availability in serum glucose (more crosses placenta)
27
Changes in CVS in pregnancy
Increase CO | Increased HR and SV
28
Changes in vessels in pregnancy
Increased CO and vasodilation by steroids = reduced peripheral resistance Increased flow to uterus, placenta, muscle, kidney and skin
29
Stages of implantation
1. Apposition 2. Attachment 3. Invasion
30
Day 7-8 in implantation time line
Blastocyst attach to the surface of decidua basalis. | Trophoblast cells assemble to form SYNCYTIOTROPHOBLAST to facilitate invasion of decidua basalis
31
Day 9-11 in implantation time line
Syncytiotrophoblast further invades the decidua basalis and by day 11 it is almost buried in the decidua
32
Day 12 in implantation time line
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
33
Day 14 in implantation time line
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
34
How are primary villi formed
Cells of syncytiotrophoblast protrude to form tree like structures
35
How are lacunae formed
Decidual cells between primary villi begin to clear out, leaving behind spaces
36
What is the junctional zone
Blood filled with lacunae merge into single large pool of blood connected to multiple arteries and veins
37
Day 17 in implantation/placenta time line
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
4th and 5th month of placenta timeline
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
Pre-eclampsia
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
Risk factors of pre-eclampsia
1st pregnancy Hypertension, diabetes, obesity Hypertension - decreased blood flow in kidney and lead to proteinuria Pre-eclampsia + seizures = eclampsia
41
Cause of Placenta abruption
Degradation of maternal arteries supplying blood to the placenta. Degenerated vessels rupture causing haemorrhage and separation of the placenta
42
Complications - maternal of placenta abruption
Hypovolemic shock Sheehan syndrome Renal failure Disseminated intravascular coagulation (from release of thromboplastin)
43
Complications - foteal of placenta abruption
Intrauterine hypoxia and asphyxia | Premature birth
44
Placenta previa
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
Risk factors of placenta previa
``` Previous caesarean delivery Previous uterine/endometrial surgery Uterine fibroids Previous placenta previa Smoking and recreational drug use ```
46
Hormonal changes in pregnancy
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
Spermatogonia
Germ cell on basement membrane, capable of mitotic or meiotic division into spermatocytes or more spermatogonia by mitosis. They are diploid
48
Primary spermatocytes
Move into adluminal compartment and duplicate their DNA into sister chromatids which exchange genetic material before entering meiosis I. 46XY diploid
49
Secondary spermatocytes
Have undergone meiosis I to give 23X + 23Y haploid number of chromosomes arranged as sister chromatids
50
Spermatids
Meiosis II occurs to give 4 haploid spermatids. Round spermatid to elongated spermatid differentiation
51
Spermatoza
Mature sperm extruded into the lumen
52
Sexual determination
Genetically controlled process dependent on the switch on the Y chromosome Chromosomal determination of male or female
53
Sexual differentiation
Process by which internal and external genitalia develop as male or female
54
Primordial germ cells become
Sperm or oocytes
55
Primitive sex cords become
Sertoli cells or granulosa cells
56
Mesonephric cells become
Leydig cells or theca cells
57
Gonadal dysgenesis - AIS
Testosterone is made but has no effect | Testis form and make AMH - regression of Mullerian ducts
58
Complete AIS
Appear female at birth but is XY - undescended testes | Primary amenorrhoea and lack of body hair
59
5 alpha reductase deficiency
Testosterone made but not DHT Testes form and make AMH - Wolffian ducts develop External structures do not develop AUTOSOMAL RECESSIVE
60
Turner syndrome
Females missing X chromosome | Uterus and tubes are present but small, other defects in growth and development
61
Congenital adrenal hyperplasia (CAH)
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
Pathway block leading to CAH
Failure to synthesise cortisol - (by 21 hydroxylase) | No negative feedback so CRH will stimulate pituitary to release ACTH
63
Regulation of uterus by neurotransmitter
Sympathetic innervation Expression of alpha and beta adrenoreceptors alpha adrenoreceptor agonist = contraction beta adrenoreceptor = relaxation
64
Regulation of uterus by sex hormones
Progesterone inhibit contraction | Oestrogen increases contraction
65
Hormones in a non pregnant uterus
Weak contractions | Strong contractions during menstruation - decrease progesterone, increase prostaglandin
66
Hormones in pregnant uterus
Weak and uncoordinated contraction - high progesterone | Strong and coordinated contraction at parturition - high oestrogen
67
Oestrogen/progesterone ratio during parturition
Increases Oestrogen increases while progesterone decreases gap junction expression in myometrium Oestrogen/progesterone also found in ICC
68
Regulation by prostaglandins
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
Prostaglandin analogues
dinoprostone (PGE2) Carboprost (PGF2α) Misoprostol (PGE1)
70
Uses of prostaglandin
Induction of labour - before term Postpartum bleeding Softening of cervix
71
Concerns of prostaglandins
Dinoprostone can cause systemic vasodilation Potential for CVS collapse PGs - hypertonus and foetal distress
72
What is oxytocin
Non-peptide hormone synthesised in hypothalamus and released from posterior pituitary gland Effective at term
73
Regulation by oxytocin
Oestrogen released after parturition produce - increase oxytocin release, oxytocin receptors and increase gap junctions. Oxytocin also synthesises prostaglandins
74
Pharmacological actions of sythetic versions of oxytocin
Low conc. of oxytocin analogue – increase frequency and force of contractions. High concentrations cause hypertonus – may cause foetal distress
75
Synthetic versions of oxytocin
Syntocinon and pitocin
76
Uses of synthetic versions of oxytocin
Induction of labour at term – does not soften cervix Treat/prevent post-partum haemorrhage Syntometrine – oxytocin (rapid)/ergot (prolonged) combination
77
Action of ergot
Powerful and prolonged uterine contractions - but only when myometrium is relaxed
78
Mechanism of ergot
Stimulate alpha adrenoreceptors and 5HT receptors
79
Uses of ergot
Post partum bleeding - not induction
80
Myometrial relaxants
May be used in premature birth - delay delivery by 48hrs
81
Beta adrenoreceptor stimulants
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
Ca2+ channel antagonist
Nifedipine Used in hypertension Or mg sulfate
83
Oxytocin receptor antagonists
Retosiban
84
COX inhibitors
NSAIDs
85
What to use for induction of labour
Oxytocin
86
What to use for Induction labour/termination in early term
Prostaglandins
87
What to use for post partum bleeding
Prostaglandins Oxytocin Ergots
88
What to use to prevent premature birth
Beta 2 adrenoreceptor agonists Ca2+ channel blockers, Mg sulphate Oxytocin inhibitors

PHYSIOLOGY 2 (5 decks)

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