embryology Flashcards

1
Q

describe the process of gastrulation; when does it occur?

A

day 15/16 PF
conversion of bilaminar disc (epiblasts and hypoblasts) to 3 germ layers (endoderm, mesoderm, ectoderm)
epiblasts migrate through the primitive streak, proliferate and differentiate into mesoderm
epiblasts -> endoderm
hypoblasts -> ectoderm

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2
Q

what tissues do the 3 germ layers develop into

A

endoderm: gut, liver, lungs
mesoderm: skeleton, muscle, kidney, heart, blood
ectoderm: skin, nervous system

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3
Q

male urogenital system development (4)

A
  1. Mesonephric ducts (Wolffian) → MALE genital ducts (SRY+)
  2. Leydig cells → testosterone → mesonephric duct growth
    hCG peak week 8 after LMP → testosterone from developing testis (critical stage of development)
  3. Testosterone → DHT → prostate, penis, scrotum
  4. Sertoli → AMH → regression of paramesonephric (Mullerian) ducts
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4
Q

female urogenital system development (4)

A
  1. Absence of SRY → ovary
  2. No testosterone → regression of mesonephric ducts
  3. No AMH → Mullerian duct persistence → oviducts, uterus, upper 1/3 of vagina
  4. Urogenital sinus → lower 2/3 of vagina
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5
Q

changes in heart at birth (2)

A
  1. Loss of foramen ovale (shunt between R & L atria)
  2. Loss of ductus arteriosus (connecting pulmonary artery & descending aorta)
    → allows use of pulmonary circulation
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6
Q

stages of lung development (6)

A
  1. Embryonic: lays down basic structure of lungs
  2. Pseudoglandular: develops gland-like structures
  3. Canalicular: becomes more elaborate
  4. Saccular: develops sacs
  5. Alveolar: sacs form alveoli (very late, around time of birth)
  6. After birth, changes continue and accelerate
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7
Q

surfactant

  1. function
  2. produced where?
  3. associated disease
  4. management
A
  1. important for low surface tension of alveoli → allows expansion of alveoli
  2. produced by type II pneumocytes
  3. Late surfactant production → respiratory distress syndrome: collapsed alveoli → insufficient oxygen
  4. Surfactant production increases w time ∴ can treat RDS by delayed delivery + allowing lungs to continue developing
    OR give glucocorticoids / artificial surfactant
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8
Q

achondroplasia

A

FGFR3: gain of function mutation → loss of elongation of long bones in limbs

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9
Q

how does thalidomide cause maldevelopment

A

thalidomide → derangement of development of blood vessels in limb buds, especially upper → loss of nutrient supply → cell death

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10
Q

fetal membranes (3)

A
  1. decidua: endometrial origin
  2. chorion: cytotrophoblast (villous origin)
  3. amnion: epithelial layer & stroma of matrix and a few cells (including reticular layer)
    basement ECM (of amnion layer) gives fetal membranes strength; holds amniotic fluid in place and prevents leakage
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11
Q

functions of the placenta (5)

A

SEBIC:

  1. separation: of maternal and fetal blood
  2. exchange: of metabolites, glucose, oxygen, amino acids etc. by facilitated diffusion, active transport, receptor-mediated etc.
  3. biosynthesis: hormones, growth factors, cytokines
  4. immunoregulation: immunological barrier between mother and fetus (limited passage of immune cells)
  5. connection: placenta anchors into maternal decidualised endometrium
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12
Q

placenta: villous development (5)

A
  1. Primary villous: cytotrophoblasts grow through syncytium
  2. Secondary villous: mesenchyme also invades
  3. Tertiary villous: cytotrophoblast layer becomes discontinuous, development of blood vessels
  4. When cytotrophoblast column reaches decidua, proliferates sideways to form trophoblastic shell
  5. Villous tree becomes progressively more elaborate; ↑branching → ↑SA for exchange
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13
Q

remodelling of spiral arteries

A

Remodelling necessary to meet demands of growing conceptus
1. Cytotrophoblasts plug spiral artery
2. Invasion of extravillous cytotrophoblast cells
3. Loss of vascular endothelium & smooth muscle cells → wide bore vessel that cannot vasoconstrict ∴ high blood flow, low pressure
Remodelling process involves NK cells, MMPs, TIMPs
Progresses to inner third of myometrium (as dedidual tissue has thinned)
4. Loss of cytotrophoblast plugs → exposure of placenta to full maternal blood flow
Late first trimester; pregnancy losses at this time: high pressure can detach conceptus from its implantation

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14
Q

growth factor families important for maternal-placental crosstalk + functions (4)

A
  1. IGFs & IGF-binding protein-1: IGF-II binds to type A insulin receptor → enhanced cytotrophoblast survival
    IGFBP-1 increased in pregnancy → excess capacity for carrying IGFs
  2. VEGFs, PDGF, PlGF:
    in early pregnancy (low oxygen levels), VEGFs → formation of blood vessels
    in last month of pregnancy, PlGF → capillaries ↑size and become closer to edges of villi → ↑transport
  3. CSF-1 / M-CSF (colony-stimulating factors): roles in human placentation unclear
  4. TGFbeta: generally produced by decidua, inhibit trophoblast invasion and MMP activity in vitro
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15
Q

when does implantation occur

A

day 7 PF

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