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LCRS 1 > Embryology > Flashcards

Embryology Flashcards

1
Q

What structure comes before blastocyst

A

Morula- a ball of undifferentiated cells within zona pellucida

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2
Q

Development from morula to blastocyst

A

Morula differentiates so inner cells differ from outer ones

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3
Q

Structure of blastocyst

A

Outer layer of trophectoderm with an inner cell mass and fluid filled cavity

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4
Q

When does blastocyst hatch from zona pellucida

A

6 days post fertilisation

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5
Q

What happens between day 6 to 10

A

Inner cells mass of blastocyst becomes bilayer disk made of hypoblast and epiblast cells

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6
Q

What is first change to bilayer disk of blastocyst

A

Gastrulation

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7
Q

What happens in gastrulation

A

Conversion of hypoblast and epiblast cells to 3 layers of germ cells

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8
Q

What are 3 layers of germ cells

A

Ectoderm
Mesoderm
Endoderm

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9
Q

Summarise gastrulation

A

Proliferation of epiblast cells into space between epiblast and hypoblasts cells which becomes endoderm cells. Then get apoptosis of hypoblast cells

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10
Q

What does ectoderm give rise to

A

Skin and nervous tissue

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11
Q

What does mesoderm give rise to

A

Muscles, blood, skeleton, heart and kidney

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12
Q

What does endoderm give rise to

A

Gut and lungs

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13
Q

What happens before end of gastrulation

A

Neurulation begins- differentiation of ectoderm to generate CNS

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14
Q

What controls neurulation

A

Notochord in mesoderm

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15
Q

What happens in junction with neurulation

A

Precursors of other tissues develop within embryo as it is converted from flattened tissue to 3D

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16
Q

What has happened by week 4

A

Precursors of all internal tissues have been laid and some external structures have begun to develop

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17
Q

Name given to extra digit

A

Polydactyly

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18
Q

What has happened to limbs by week 8

A

Limbs roate to definitive orientation resulting in helical pattern of lower extremity dermatomes

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19
Q

Link between thalidomide and limb deformties

A

Thalidomide was given to treat morning sickness. Morning sickness normally starts around 6 weeks which matches the main stages of limb development

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20
Q

How did thalidomide affect developing limbs

A

It damaged the developing blood vessels which were supplying them with the nutrients required for proper growth and development.

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21
Q

3 stages to kidney development

A

Pronephros-most immature form
Mesonephros- intermediate phase
Metanephros- most developed and persists as adult kidney

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22
Q

Where do gonads arise from

A

Intermediate mesoderm within urogenital ridges of embryo

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23
Q

Where do male genital ducts arise from

A

Mesonpehric ducts

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24
Q

Where do female genital ducts aruse from

A

Paramesonephric ducts

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25
Q

What determines differential development of male reproductive system

A

SRY on Y chromosome

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26
Q

Describe movement of kidney during its development

A

Ascends from near to bladder- ureters extend at same time as kidney ascends to maintain connections

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27
Q

Describe changes in vascular supply of kidney during development

A

Forms new connection with developing arterial system as it moves upwards- renal arteries are broken and reformed

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28
Q

Common kidney development abnormalities

A

One kidney may be retained in the pelvis
Retention of an artery may obstruct the ureter
Kidneys form seperately but then fuse to form horsehoe kidney

29
Q

What covers gonad precursor

A

Colemic epithelial cells

30
Q

What gives rise to gametes within gonads

A

Primordial germ cells

31
Q

What regulates male development of urogenital tract

A

Testosterone from Leydig cells

32
Q

What stimulates testosterone from leydig cells during development

A

hCG from maternal circulation- hCG levels peak around 7-8 weeks when this development starts

33
Q

What do sertoli cells produce to regress Mullerian ducts

A

AMH- anti mullerian hormone

34
Q

Differentiation of tracts to either male or female

A

Around 9 weeks the indifferent genitalia are converted to either male or female. This is regulated by DHT produced from testosterone originating in Leydig cells of testis

35
Q

What are most mal-developments as a result of in males

A

Inability to produce AMH or testosterone

Inability of target organs to respond to these hormones

36
Q

What causes Androgen insensitivity syndrome

A

Mutant androgen receptor in males

37
Q

Effects of androgen insensitivity syndrome

A

Limited virilisation of external genitalia
Testis sructure is viable but do not descend
Mesonephric ducts are lacking

38
Q

Why do paramesonephric ducts regress and no female structures are present

A

Can still produce AMH

39
Q

What causes congenital adrenal hyperplasia

A

Mutant 21a hydroxylase enzyme

40
Q

Effect of CAH

A

Lack of cortisol means no negative feedback on ACTH which remains high. This leads to overstimulation of adrenals causing an increase in weaker androgens. This results in partial virilisation of female genitalia

41
Q

Why are internal systems normal in females with CAH

A

no SRY

42
Q

Why are there no male ducts in females with CAH

A

No testosterone

43
Q

Why do female ducts develop normally in CAH

A

No AMH as no sertoli cells

44
Q

Describe cardiac embryology until the 21st day

A

Cardiogenic cells develop in a U pattern outside the proper embryo to form a pair of heart tubes. These fuse by day 21 and are able to pump blood unidirectionally

45
Q

What gives rise to the 4 chambered structure

A

Looping and septation

46
Q

What happens during looping and septation of the heart

A

Vascular connections are made eg veins to atria and valves develop

47
Q

2 differences in structure of heart pre-delivery and after

A

Presence of foramen ovale which is gap between 2 atria

Presence of ductus arteriosus between right ventricle and left ventricle

48
Q

Reason for foramen ovale

A

Allows blood passing from right atria to left atria to limit blood flow out of the right ventricle to lungs

49
Q

Reason for ductus arteriosus

A

Blood flowing to lungs instead flows to rest of body through left ventricle

50
Q

4 abnormalities assocaited with tetraology of fallot

A
  1. Pulnomary stenosis
  2. Thickened right ventricle wall
  3. Ventricular septal defect
  4. Overriding aorta
51
Q

What is pulnomary stenosis

A

Narrowing of pulnomary valve

52
Q

What is the ventricular septal defect in tetralogy of fallot

A

Hole in the wall of right ventricle

53
Q

What is overriding left ventricle

A

Aorta is shifted to right and recieves blood from both ventricles

54
Q

What causes blue baby syndrome

A

Babies become cyanotic as there is transposition of aorta and pulnomary artery meaning right ventricle pumps out deoxygenated blood to rest of body

55
Q

What happens in spina bifida

A

Fusion of the neural tube should have happened by 3 weeks but in spina bifida there is a failure of fusion in an area and it leads to exposure of spinal chord above skin

56
Q

Result of spina bifida

A

Inability to walk
Damage to tissues associated with supply from that area
Varies a lot between patients

57
Q

Cause of spina bifida

A

low maternal folate diet

58
Q

Where do facial structures develop at what period

A

After 5 weeks the primary structures are on the side of the face and move centrally over the next 5 weeks

59
Q

What happens to facial features as they migrate medially

A

Clefts are formed and these are then filled by fusion of the tissue from either side

60
Q

How do you get cleft palates and lips

A

Incomplete fusion of tissues from either side of the face

61
Q

Is cleft palate normally asymmetric or not

A

symmetric

62
Q

Is cleft lip normally asymmetric or symmetric

A

asymmetric

63
Q

5 steps to lung development

A 
Embryonic
Psedoglandular
Canalicular
Saccular
Alveolar
64
Q

Describe lung development

A

Starts at bronchi and ends at alveoli

Effective moves all the way along

65
Q

When does surfactant production begin

A

Start of third trimester

66
Q

Why is surfactant production so important

A

Necessary for lung function when exposed to air

67
Q

What lung condition do some preterm babies suffer from

A

Respiratory distress syndrome

68
Q

What causes RDS

A

lack of surfactant

69
Q

What can be given to increase surfactant production in babies who are going to be preterm

A

Glucorticoid injection to mother as accelerates production

Artificial surfactant has been developed that can be injected into babies

LCRS 1 (58 decks)

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