Block 11 key things to learn

Question 1

What is the polar body and when is it formed?

Answer 1

Second meiotic division is uneven and extrudes a polar body to get rid of chromosomes that aren’t needed.
Presence of it means fertilisation has occurred

Question 2

What do foetus and placenta work together to produce?

Answer 2

Oestrogens- foetus make C19 androgens and placenta converts it to oestrogen

Question 3

What drugs have fetotoxic effects in the 1st trimester?

Answer 3

Androgens- visualisation of female foetus
Oestrogen- feminisation of male foetus
Warfarin- nasal hypoplasia and skeletal defects
Retinoids- craniofacial, CVS and CNS defects
Diethylstillboestrel- uterine lesions, transplacental carcinogen
Anti-epileptics- facial defects, mental retardation, neural tube defects

Question 4

What drugs have fetotoxic effects after the 1st trimester?

Answer 4

Anti-epileptics- mental retardation
Narcotics- respiratory depression
Warfarin- foetal haemorrhage, CNS abnormalities
Antidepressants- neonatal withdrawal
Benzodiazepines- floppy infant syndrome
withdrawal, respiratory depression

Question 5

What do ACE inhibitors cause in the foetus?

Answer 5

Oligohydraminous, growth retardation, lung and kidney hypoplasia, hypocalvaria, neonatal convulsions, hypotension and anuria

Question 6

What are some issues of where foetal circulation doesn’t adapt after birth?

Answer 6

Duct dependent systemic circulation-
coarctation of aorta
critical aortic stenosis
hypo plastic left heart syndrome

Duct dependent pulmonary circulation-
pulmonary atresia
critical pulmonary stenosis
tricuspid atresia
teratology of ballot

Duct dependent systemic and pulmonary circulation-
transposition of great arteries

Question 7

What happens in capacitation?

Answer 7

Needs time away from seminal fluid, led by calcium.

2 parts-

• hyperactivation- sperm starts swimming
• removal of acrosomal cap so fertilisation can occur

Question 8

What happens in fertilisation?

Answer 8

Acrosomal head of sperm has enzyme hyaluronidase to digest through cumulus cells surrounding egg to get to zona pellucida.
Then sperm interacts with proteins ZP2 and 3 to trigger acrosome reaction and sperm gets incorporated into egg.
Then trigger hardening of zona to block polyspermy

Question 9

How does the egg get activated?

Answer 9

Sperm contributes DNA and phospholipase C gamma.

Enzyme starts calcium signalling cascade needed to activate egg and trigger 2nd meiotic division

Question 10

How does blastocyst implantation occur?

Answer 10

Uterine epithelium produces heparin binding epidermal growth factor and signals to embryo to produce epidermal receptor so embryos can attach to uterine epithelium.

Embryo then produces enzyme serine I theonine kinase to change the endometrium so it can implant

Question 11

What are the 4 pelvis types?

Answer 11

Gynecoid- 50% of women, wide pubic arch- good for delivery
Android- narrower pubic arch, harder delivery
Anthropoid- wider anterior-posterior direction but narrower across so issue with rotation- baby born back to back
Platypelloid- same as above but wider across ways

Question 12

What are the forces of retention in labour?

Answer 12

Progesterone
Hypervolaemia
Relaxin
CRH
Adrenaline
Cervix

Question 13

What are the forces of release in labour?

Answer 13

Oestrogen
Oxytocin
Vasopressin
Prostaglandins
Cortisol
Uterine distension

Question 14

What is looked at in the postnatal examination?

Answer 14

W- wound assessment 
O- observations
M- monitor first urine void
A- assess uterus
N-note colour and circumference of calves

Question 15

What is looked at in the newborn APGAR?

Answer 15

Activity
Pulse
Grimace
Appearance
Respiration

Question 16

What is the UK vaccination schedule?

Answer 16

8 weeks- 6 in 1, pneumococcal, rotavirus, menB
12 weeks- 6 in 1, rotavirus
16 weeks- 6 in 1, menB, pneumococcal
1 year- hib/ menC, MMR, MenB, pneumococcal
2-9 yrs- Annual flu jab
Preschool- 4 in 1, MMR
13 yrs girls- HPV x2
14 yrs- 3 in 1 , MenACWY

Question 17

How does foetal mammogenesis occur?

Answer 17

Derived from ectoderm and mesoderm layers

Starts as 2 milk streaks from axilla to groin then thickens and become glandular tissue that grows into chest. Then get mammary bud branching and differentiation of smooth muscle cells of nipple cells etc.
Then have primary milk ducts by 32 weeks gestation which open up onto nipple and nipple and areola develop and become pigmented

Question 18

What is the nerve and blood supply of the breasts?

Answer 18

Intercostal nerves
Arterial supply from internal mammary artery and 30% from lateral thoracic artery
Venous drainage from internal and external mammary and axillary veins

Question 19

What are the stages of lactogenesis?

Answer 19

I- Mid/ late gestation- 48 hours after birth
Endocrine control
Some colostrum made in alveoli and fat droplets accumulate in lactocytes
Colostrum produced is proportional to prolactin but prolactin is inhibited by high progesterone levels

II- Triggered after labour finished and oestrogen and progesterone levels fall
Tight junctions between lactocytes close and mum feels breast fullness 2-3 days after birth
Breast milk sodium and protein levels fall but lactose and lipids rise
Change to aubocrine process

III- from day 8-9
Process is aubocrine control
Milk removal drives production

Question 20

What are the theories of lactation?

Answer 20

Prolactin receptor theory-
Prolactin receptors in lactocytes distort shape when breast full off milk so prolactin can’t attach so less milk is produced, so prolactin can only attach when don’t have much milk made

Feedback inhibitor of lactation-
small whey protein in breast milk slows milk synthesis when breasts are full

Prolactin inhibitory theory-
Hypothalamic factor build up and suppresses prolactin secretion from anterior pituitary when breasts are not emptied to decrease milk production and vice versa

Question 21

How is milk ejected?

Answer 21

Suckling causes release of oxytocin from posterior pituitary which travel via blood to breast to stimulate myoepithelial cells to contract and squeeze milk out of breast

Question 22

What are the mediators of growth?

Answer 22

Growth hormone from anterior pituitary stimulates growth at epiphyseal plates.
Also have indirect actions mediated by insulin like growth factors- IGF1 which is stimulated by GH after birth.

But iGF II is independent of GH and if over expressed in foetus then get large tongue, muscles, heart liver and kidney

Question 23

How is growth hormone regulated?

Answer 23

GH stimulates IGF1 from target tissue
IGF1 directly inhibits GH release by suppressing somatoptrophs
Also indirectly inhibits GH release by suppressing GNRH release from arcuate nucleus of hypothalamus
GH also inhibits its own release via short loop feedback on somatotropin

Question 24

Describe achondroplasia?

Answer 24

Most common form of dwarfism
Autosomal dominant mutation in chromosome 4 coding for FGFR3
Causes decreased endochrondral ossification and inhibits proliferation of chondrocytes in growth plate cartilage and epiphyseal growth plate closes early

Average height 120-125cm
All organs normal
Large head, prominent forehead, flat bridge of nose, short hands, stubby fingers

Question 25

Acromegaly?

Answer 25

Hypersecretion of GH usually due to adenoma of somattroph cells
GH secreted constantly no diurnal variation
In children have excess long bone growth
In adults all organs are affected and they have increased lip size, liver size, skin thickness and sweating

Usually glucose inhibits GH release, but not in acromegaly

Question 26

Pituitary hypothalamic defiency?

Answer 26

GH deficiency in childhood - pituitary dwarfism
May be accompanied by low levels of other pituitary hormones
Causes- infection, pituitary tumour, vascular malformation or head injury
Recombinant GH therapy allows some catch up

Question 27

Laron dwarfism?

Answer 27

Mimics GH deficiency
Actually due to mutation in GH receptor
So lots of GH but low levels of IGF1- results in growth retardation
Same short stature and appearance of those who lack GH
Treat with recombinant IGF1