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Krishan RDA > Embryology > Flashcards

Embryology Flashcards

1
Q

Oxygen tension in 1st trimester?

A

Low - 3% to prevent production of free radicals

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2
Q

Summarise Embryology in 1st trimester 3-8 weeks?

A
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3
Q

Embryological timings v,s gestational timings?

A
  • Embryological timings are usually about 2 weeks less than the gestational time frames.
    • E.G. 12 weeks GA is 10 weeks embryologically.
    • GA time frames – starts after the beginning of the last menstrual period.
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4
Q

What is development measured in?

A

Carnegie stages.

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5
Q

Define Blastocyst, Embryo, Foetus, Conceptus?

A
  • Blastocyst – epiblast and hypoblast present at ~9 days
  • Embryo – small developing conceptus present at ~5-6 weeks
  • Foetus – developing conceptus present at ~3 months for rest of prgenancy.
  • Conceptus – anything derived from a fertilised egg
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6
Q

What is the red part in the image?

A

the red part is the liver developing and is where the RBCs are made before the spleen kicks into action.

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7
Q

The body repeats what 4 simple processes to achieve embryology.

A
  • Cells must – proliferate, move, differentiate & be able to undergo cell loss.
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8
Q

Regulation of Cells in development - signalling methods and concentration signalling?

A
  • Signalling methods:
    • Paracrine – to adjacent cells.
    • Autocrine – to oneself.
    • Endocrine – over long distances via vasculature**.
      • During embryo development, there isn’t much vasculature made so this doesn’t occur much.
  • Concentration signalling – the strongest signals are received by cells located closest to the source of the signalling molecules.
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9
Q

Concentration signalling – the strongest signals are received by cells located closest to the source of the signalling molecules.

So what happens if the source cells are at the tip?

A
  • If the source cells are at the tip, the highest levels of proliferation will remain at the tip and thus a “bud” will form towards the apex – e.g. a limb bud.
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10
Q

Asymmetrical development can occur how?

A
  • With +ve stimuli and –ve stimuli, asymmetrical development can also occur…
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11
Q

Embryology depends on what?

A

gradients of factors, combinations of factors, temporal changes in factors or responses to them.

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12
Q

Name a gene important in the regulation of development?

  • what it does, how is it activated
A
  • Genes regulate development heavily:
    • HOX genes – establish A-P (Anterior-Posterior) axis, differences in the vertebrae, CNS divisions, patterns in the limbs.
    • Activation of HOX is controlled by retinoic acid, a derivative of vitamin A.
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13
Q

Embryology Timeline: The conceptus starts as?

A
  1. The conceptus starts as a bilaminar disc inside a blastocyst – comprised of an epiblast and a hypoblast layer.
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14
Q

What process forms a 3-layer conceptus?

A
  1. Gastrulation forms a 3-layer conceptus – the ectoderm, mesoderm and endoderm.
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15
Q

What structures do the 3 layers formed in gastrulation form?

A
  • Endoderm = gut, liver and lungs.
  • Mesoderm = skeleton, muscles, kidneys, the heart and blood.
  • Ectoderm = skin and the CNS.
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16
Q

Describe how gastrulation = 3 layers?

A
  1. Epiblast proliferates = a group of cells that infiltrate the space between epiblast and hypoblast (primitive streak)
  2. mesoderm cells cause hypoblast cells to apoptose and differntiate = endoderm cells.
  3. so thought that epiblast forms all 3 germ layers
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17
Q

After gastrulation has formed 3 layers what happens?

A
  • After gastrulation has formed 3 layers, the ectoderm proliferates to form the neural plate (with NO proliferation at the neural groove – negative stimulation of notochord) and the neural fold’s fold over and form the neural canal.

The body cavity then closes by day 28 and pinches off the yolk sac into the umbilical cord

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18
Q

How does the neural fold = canal and explain closure of - the neural tube closes by week 4?

A
  • The tissues will fuse down the midline leaving just 2 openings at the anterior neuropore and the posterior neuropore.
  • During days 25-28, the neuropores SHOULD close.
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19
Q

Types of Spina bifida – TOP = bad prognosis to good prognosis (bottom)

A
  • Myelomeningocele – neural tissue in bulge.
  • Meningocele – no neural tissue in bulge.
  • Spina bifida occulta – hair growth over area affected, no growth.
  • Note: The fact that there is no formation of vertebrae at the bulge suggests that bone growth is dependent on neural tissue growth.
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20
Q

What can be interpreted from the fact that

Myelomeningocele – neural tissue in bulge.

Meningocele- no neurl tissue in bulge?

A
  • The fact that there is no formation of vertebrae at the bulge suggests that bone growth is dependent on neural tissue growth.
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21
Q

Heart begins to develop at week 4 explain heart development?

A
  1. The two endocardial tubes fuse into a primitive heart tube that pumps blood.
    1. Endocardial tubes develop in the mesoderm and come together as the body cavity closes (pinching off of yolk sack = umbilical chord)
    2. Note: primary and secondary heart field form into the primitive heart tube by fusing and then breaking the arch at the apex - to allow blood to go through.
  2. The heart then undergoes a turning action (anti-clockwise) to form the primitive heart and the 4 chambers form.
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22
Q

describe - The heart turning action?

  • What aids the heart movement?
A
  • The primitive heart tube undergoes an anti-clockwise turning motion which results in the ventricles being at the bottom with the atria at the apex.
  • The atria rotate BEHIND the arteries.
  • The head-tail folding is also occurring which aids rotation of the heart and the movement of the heart more internally.
23
Q

Role of the ductus arteriosus and patent foramen ovale?

A
  • At birth, the ductus arteriosus and foramen ovale close to shift the heart from a single cycle flow in the foetus to a figure of eight loop flow.
  • The ductus arteriosus and patent foramen ovale act as shunts to the blood supply (so that the blood avoids the pulmonary system).
24
Q

How to limbs develop and when?

A

Limb Development [aprox 4 weeks]

  • The forelimb bud appears at day 27/28, hind limb bud at day 29.
  • Budding is growth from the lateral plate mesoderm which is done rapidly under control of special signalling regions.
25
Q

What is Achondroplasia?

A
  • Achondroplasia – FGF23 gain of function mutation:
    • Concerns the elongation of limbs and not primary formation, they just aren’t long limbs.
    • The mutation stops conversion of cartilage to bone.
26
Q

Effecs of thalidimide on embryology?

A
  • Mainly affected limbs but also – eyes, heart, alimentary/urinary tracts, blindness and deafness.
  • CURRENTLY used to treat leprosy and some cancers.
27
Q

How does thaladimide cause abnormal embryology?

A
  • Thalidomide:
    • Interferes with the blood vessel development which led to apoptosis and death of developing cells.
28
Q

Another condition that can affect limb development?

A

polydactyly.

29
Q

Role of Shh – Sonic Hedgehog protein?

A

Polarising factor for limb development.

30
Q

Role of Pronephros?

A
  • Pronephros – develops first, precursor tissue:
    • As Mesonephros forms, the Pronephros is degenerating.
    • Has NO excretory function, solely developmental.
31
Q

Function of Mesonephros?

A
  • Mesonephros – connects to cloaca, limited excretory function.
32
Q

Comon feature of pronephros + Mesonephros

A
  • Both pro- and meso-nephros have small tubules that stick out.
33
Q

UGS development After the mesonephros has formed, what two things happen?

A
  • Metanephric ducts grow out of the cloaca and begin to form the kidneys.
  • Mesonephric ducts begin to differentiate into gonads (testes) – ducts mainly apoptose in females.
34
Q

Explain vascular development of kidney?

A
  • Vascular buds initially grow from the kidney and invade the common iliac arteries.
  • As the kidneys ascent cranially, the kidneys DON’T drag the blood supply (like testes decent) but form new vessels and then induce regression of old vessels.
35
Q

Explain Bladder development?

A
  • Bladder (from cloaca) development:
    • Endoderm à bladder – except for the trigone (mesodermal) which develops from mesonephric duct.
    • Trigone signals filling of the bladder.[The area is very sensitive to expansion and once stretched to a certain degree, the urinary bladder signals the brain of its need to empty].
36
Q

Kidney developmental errors?

A
  • Renal agenesis – degeneration of ureteric bud:
    • Unilateral – L>R.
    • Bilateral – “Potter’s syndrome” – Oligohydramnios.
  • Abnormal shaped kidneys.
  • Abnormal ureter – bifid ureter {ureter splits into 2], double kidneys [2 ureters] , supernumerary kidney (extra kidney).
  • Pelvic or horseshoe-shaped kidney – kidney doesn’t ascend or kidneys fuse caudally to horseshoe shape.
  • Bladder exstrophy [bladder inside out - i.e exposed on body]
37
Q

Development of the male and female ductal system?

  • talk about germ cells
A
  • Paramesonephric duct – Mullerian ducts = female ductal systems.
  • Mesonephric duct – Wolffian duct = male ductal systems.
  • The cells that give rise to gametes are primordial germs cells (give rise to eggs and sperm) and are found outside the embryo in the yolk sac to begin with and then they MOVE INTO THE EMBRYO and then move into the gonads (gonads are “indifferent” before the PGCs move in and they are identical in males and females to begin with).
38
Q

Male ductal system develops from the mesonephric duct under the influence of what?

What becomes the testes?

Explain the difference in females?

A
  • Male ductal system develops under influence of SRY gene.
  • Mesonephric ducts begin to differentiate into gonads (testes) – ducts mainly apoptose in females.
  • Female – the mesonephric duct is NOT connected to the ovaries and it has developed separately [from Paramesonephric ducts].
39
Q

Summarise testits development?

A

SRY expression: a gonad develops into a TESTIS containing spermatogonia, Leydig cells, and Sertoli cells.

Leydig cells produce TESTOSTERONE, which support growth of the mesonephric ducts. NOTE: without testosterone, the mesonephric ducts will regress [hCG drives testosterone production from the Leydig cells (which usually respond to LH).].

Some testosterone is converted into Dihyroxytestosterone (DHT), which supports development of the prostate gland, penis, and scrotum.

Sertoli cells produce ANTI-MÜLLERIAN HORMONE (AMH, or Müllerian Inhibiting Substance, MIS), which induces regression of the paramesonephric ducts. NOTE: in the absence of MIS, the paramesonephric ducts will persist.

40
Q

Summarise Female RT development?

A

Female RT: In the absence of SRY, the gonad develops into an ovary with oogonia and stromal cells.

Since no testosterone is produced, the mesonephric (Wolffian) ducts regress.

Since there is also no ANTI-MÜLLERIAN HORMONE , the Müllerian (paramesonephric) ducts persist to give rise to the oviducts, uterus, and upper 1/3 of the vagina

The urogenital sinus contributes to the formation of the bulbourethral glands and the lower 2/3 of the vagina

  • Ureteric bud – ureter.
  • Mesonephric ducts – trigone of bladder.
41
Q

MAle UGT?

Ureteric bud - forms what

Mesonephric ducts

Urogenital sinus

A
  • Summary:
    • Ureteric bud = ureter.
    • Mesonephric ducts = rete testes, efferent ducts, epididymis, vas deferens, seminal vesicle, trigone of bladder – ANYTHING IN TESTES AND TRIGONE.
    • Urogenital sinus = bladder (- trigone), prostate gland, bulbourethral gland, urethra.
42
Q

Explain testes decent?

A
  • Descent of the testes:
    • Arise in lumbar region and descend into pelvic cavity via inguinal canal.
    • Descent is due to tethering of testes to anterior body wall by the gubernaculum. Growth and elongation of embryo coupled with shortening of gubernaculum pulls testes through body wall.
43
Q

reasons for Abnormal development?

A

Abnormal development – structural or due to changes in or responses to, hormones.

44
Q

What is Hypospadias?

A

fusion of urethral folds’ incomplete – urethra exits penis early.

45
Q

Mullerian duct anomalies and give an example?

A
  • Mullerian duct anomalies (abnormal fusion of ducts) – e.g. two uteruses.
  • Note: Paramesonephric ducts (Mullerian) give rise to – oviducts, uterus, upper 1/3rd of vagina.
46
Q

Persistent Mullerian duct syndrome (males)?

A
  • Occurs in males with mutations in Anti-Mullerian Hormone or receptor.
    • No inhibition so paramesonephric ducts persist.
    • Testis either sit by ovaries or one/both can descend.
  • Testosterone/DHT is produced so normal external genetalia/ducts.
47
Q

Androgen Insensitivity (“Testicular Feminisation”) Syndrome (males)?

A
  • Occurs in genetic (XY) males with mutations in the androgen receptor.
  • Lack of virilisation (androgens have no effect on receptor).
    • Normal female external genetalia but undescended testes.
    • Mesonephric ducts rudimentary due to loss of testosterone.
    • Normal production of Anti-Mullerian Hormone from Sertoli cells causes Mullerian duct regression so no oviducts, uterus or upper 1/3rd of vagina.
48
Q

Congenital adrenal hyperplasia?

A
  • Congenital adrenal hyperplasia:
    • Occurs in genetic females with no 21-OH enzyme (no cortisol).
      • Causes overproduction of ACTH and overactive adrenal glands.
    • Leads to increased weak androgen production (DHEAS) = weak virilisation.
      • Enlarged clitoris, partial or complete labia majora fusion.
    • Internal genetalia are all female – testes absent (no SRY), No testosterone is produced so mesonephric tubes (Wolffian tubes) regress., no AMH/MIS so Mullerian (paramesonephric) ducts persist.
49
Q

Describe Lung development?

  • refer to specific developmental phases
A

Lungs: gradual development of tubular system from week 3 post fertilisation.

Embryonic phase - lung buds and main bronchi

Pseudoglandular Bronchi and bronchioles

Bronchioloes expand and get more specific in the canalicular period;

Epithelial cells of lung come into direct contact with capillaries in saccular period; alveolar development can overlap with saccular; some parts may be ahead of other regions.

  • surfactant produced at week 25 PF

At birth there is a key change in lung structure -> need to produce enough surfactant otherwise lungs can’t inflate and collapse.

Surfactant: lipids, proteins and glycoproteins

Is in response to glucocorticoids, and signifies to the placenta when detected to initiate labour

In utero production can be increased by 1 injection of glucocorticoids (2-3 days)

50
Q

Surfactant?

  • what is it
  • Produced when
  • In response to what
  • what cells produce it and function
A

Surfactant: lipids, proteins and glycoproteins

25 weeks PF

Produced in response to glucocorticoids, and signifies to the placenta when detected to initiate labour

  • Produced by T2 pneumocytes.
  • Function – induce low surface tension in the alveoli.
51
Q

What is respiratory distress syndrome?

  • treatment
A

Respiratory Distress Syndrome – Low physiological surfactant levels in foetus.

In utero production can be increased by 1 injection of glucocorticoids (2-3 days)

52
Q

Development & Mal-Development – Teratogens:

A
  • Development of detailed structures – “patterning”.
  • Teratogens are factors that dysregulate patterning.
    • Major defects occur if teratogens are present earlier in development.
    • Teratogens – drugs, radiation, infections.
      • Most exert their main effects in the 1st trimester of pregnancy.
53
Q

Face development - cleft lip and pallate?

A
  • Cleft lip and palate show failure to correctly form the face.
  • Development the face involves grooves forming in the face which should normally fill in (don’t fill in when you have clefting).
    • Faces start developing with the eyes either side of the head (near to the ears)
    • The nose also starts off developing relatively laterally
    • The movement of structures medially requires that clefting occurs in the middle of the face
    • In a cleft lip/palate, the cleft hasn’t been filled in properly.
      • The “pink” mesenchyme must disappear (apoptose) and this pulls the eyes and nostrils towards the midline.
      • The grooves are filled in by bulk tissue movement (not wound healing).
  • Clefting can be fixed well with surgery

Krishan RDA (7 decks)

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