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Mark Hill's site for this lecture

Lecture objectives

  • Understanding of hormone types
  • Understanding of endocrine gland development
  • Understanding of endocrine developmental functions
  • Brief understanding of endocrine abnormalities

We talk about hypothalamus, pituitary and adrenal, as well as other endocrine organs (thyroid gland, parathyroid gland, pancreas, adrenal glands, ovary/testicles). In the diagram, note that the pineal gland is missing. Gonads are important in both pre and postnatal sexual development.

Recall the hormone types from the past lecture.

You need to remember that the foetal endocrine glands are functional from the second trimester, and the function is critical to the development of the baby (teratology can mess this up).

Endocrine origins

  • Originate as epithelia (parenchyma - function) and mix with mesenchyme (stroma - CT and blood vessels - structure).

Hormones

  • Two basic classes of signalling: 1) Cell surface receptors (e.g. peptides) and 2) Cytoplasmic/nuclear receptors (e.g. steroidal)
    • In both cases, these hormones can only act on cells that have receptors for them

Pineal gland

  • Noted by arrow, the posterior anatomic equivalent of the pituitary gland
  • Secretes melatonin; cells are called pinealocytes
    • Regulates diurnal rhythm, and is important in the development of the genital system (inhibits secretion of GnRH until puberty). After puberty, the gland regresses
  • There are other possible roles of the pineal gland (unconfirmed)

Origin

  • Neuroectoderm - comes from the prosencephalon (forebrain) that then goes on to form the dienencephalon
  • There is a small median outgrowth, then forms a hollow epithelial body (neuroectoderm), that then becomes solid
  • The pineal gland is a mixture of astrocytes, pinealocytes and neurons

Hypothalamus

  • Comes from the front of the forebrain region; at the level of where the optic stalk is coming off from the diencephalon
  • Also neuroectoderm in origin; basically the same origin as the pineal gland
    • Forms as median diverticulum from the floor of the neuroectoderm of the forebrain
  • Mamillary bodies form laterally
  • Purple picture is week 5 (stage 13)
  • Beginning of its hormone secretion is in the second trimester
  • In the 8th week (Stage 22) we see the optic chiasm is closely related anteriorly to it

Pituitary (hypophysis)

  • Also ectodermal in origin
  • Left hand image: stage 13 embryo
    • Arrow up = roof of developing oral cavity; in close association with the floor of the neural tube. This roof of the oral cavity is a part that lay outside the buccopharyngeal membrane (so it's ectodermal, not endodermal, which would have been inside the buccopharyngeal membrane). This indentation is called Rathke's pouch
    • Arrow down = floor of the pharynx, and the developing cells on the surface of the floor that develop the thyroid gland. These cells are inside the buccopharyngeal membrane (so it's endodermal in origin).
  • Animation shows the events occurring in normal hypophyseal development
    • Floor of the neuroectoderm pockets downwards as the roof of the oral cavity pockets upwards. Hence posterior pituitary = neuroectoderm, and anterior pituitary = surface ectoderm. The pars intermedia is a remnant of Rathke's pouch.
    • The blue stalk downwards is the stalk of the hypothalamus
  • Week 12 picture shows the pituitary developing in the cartilaginous space called the sella turcica, an indentation in which the pituitary forms (later this "saddle" becomes bone).
    • This space is in the sphenoid bone (part of the chondrocranium). Just anterior to the pituitary is the optic chiasm, and in front of that is the lamina terminalis (where the neural tube initiall closed)
  • We can see Rathke's pouch very early on (week 3, 4). See the pituitary timeline
    • Towards the end of embryonic development the connection of neuroectoderm with surface ectoderm is lost (hence unlikely to have an abnormality in this communication)
    • In week 8 and 9, can already see pituitary hormones being produced (it stains). Week 10, can identify foetal growth hormone and foetal ACTH.
    • Peak in TSH at week 22 (stimulating the thyroid)
    • Second surge in TSH at birth, important in postnatal survival (heat generation)

Thyroid

  • Floor of the oral cavity, we can see dark spots (in the H&E diagram left)
    • There is a hypopharyngeal eminence that pushes up from the floor of the pharynx, a small population of thyroid cells (the dark cells) that can be stained. As they proliferated, they do so as a column of cells downwards.
    • The original site of this proliferation is the foramen caecum, the initial site of descent of thyroid cells
    • The region where it descends into the neck is a site for abnormalities (thyroglossal duct, the path of descent of cells). When they reach their anatomical location, they proliferate, forming the two lobes and isthmus of the thyroid.
    • By the end of week 8, the thyroid is in its anatomical location and proliferating, in front of the trachea
    • Sometimes there is a third lobe in the anterior (isthmus)
  • Thyroglossal duct forms a hollow epithelial tube initially. As the cells proliferate, it solidifies and the communication to the oral cavity is lost
    • If not lost, you get a fistula or cysts in the neck
  • By week 11, we see accumulation of colloid in the thyroid follicles (starting to form thyroid hormone), this is stimulated by TSH from anterior pituitary
  • Foetal thyroid hormone is critical for neurological development. Many parts of the brain depend on this hormone at critical times, or else neurological abnormalities happen. Iodine deficiency (maternal diet) leads to neurological defects (cretinism - lack of neural development that can't be corrected for). WHO supplement the diet of mothers in low-salt environments
  • Surge in hormones postnatally, to support transition to external development

Parathyroid gland

  • Close to the thyroid gland, but has a different embryonic origin
  • Pharyngeal arch pouches - endodermal pockets; these are key sites of endocrine gland development
    • Parathyroid is from pouch 3 and 4 (3: inferior and 4: superior). During growth of the pharyngeal arches, the second one overgrows the lower ones, and the relative positions of the inferior arches reverses, so 3 is inferior, 4 is superior.
  • Foetal parathyroids have a critical role in regulating calcium/phosphate levels (important for bone formation and for cell signalling)
  • Parathyroid hormone is produced by the parathyroid gland, which starts secretion at week 10-12

Thymus

  • Endodermal in origin, at floor of 3rd pouch
  • Important in maturation of thymocytes, and important for haemapoeitic cells in development (no bone marrow)
  • Parathyroid cells can sometimes be displaced into thymus, confusing anatomy

Pancreas

  • Not a pharyngeal arch structure
  • Exocrine (amylase, other enzymes - works postnatally (with eating); but starts producing prenatally (late foetal period))
  • Endocrine begins prenatally.
  • Pancreatic islets form initially as buds of the surface epithelium (that is endoderm).
    • The remaining tissue is exocrine
    • Exocrine secretory part is formed from mesenchyme (into which the endoderm grows, and around which endoderm wraps)
    • Exocrine ducts are formed from endoderm
  • There are two buds of the pancreas, anterior and posterior. This same process happens in both buds, and they join together later

Pancreatic islet cells

  • All have different locations in the pancreatic islets
  • Affected in diabetes
  • Abnormal maternal blood sugar can impact on development of islets
  • Pancreatic hormones are important in development. Sugar levels of the foetus are independent of those of the mother. Mother is insulin-resistant (maintaining high maternal blood sugar).
  • Developing pancreas in week 8 is nestled between duodenum and stomach, is a tubular structure

Pancreatic islet functions

1% of total mass of the pancreas

You detect manufacture earlier on than

Adrenal

  • Cortex and medulla have different embryonic origin
  • Cortex (foetal, different from adult) originates as mesothelium (lining of peritoneal cavity region). Replaced later with adult cortex
  • Adrenal development cartoon.
    • Early stage, see neural tube, neural crest cells
    • Notochord black, aorta in red
    • Population of mesothelium migrate forward to form the cortex
    • Neural crest cells migrate down adjacent to the neural cells - some over somites, some between somites (the ones that migrate between somites go down to form the sympathetic chain, and a subpopulation continue to migrate ventrally to accumulate adjacent to the cortical region - to form the medulla)
    • Branch of aorta (adrenal artery), juts out to vascularise the organ
    • Late foetal period, begin to see appearance of adult cortex
  • Birth: have the zona glomerulosa and zona fasciculate in the cortex
    • Zona reticularis can only be seen later at year 3 (long period of differentiation of this organ)
  • Adrenal medulla does NOT get replaced (cells remain as they already are - from neural crest)

Gonads

  • Two different axes, depending on gender
  • LH and FSH are the same in both cases
    • Male - gonads produce testosterone (+precursors)
    • Female - form oestrogen and progesterone
  • Gonad forms from:
    • Mesoderm (mesothelium)
    • Gonadal ridge - mesothelium thickening from medial mesonephros
    • Primordial germ cells - from the junction of hindgut and yolk sac. When genital ridge forms, primordial germ cells migrate into genital ridge and populate them
      • Different origin to follicular cells (female) or __ cells (male)

Testes

  • If testosterone and androstenedione are not secreted by Leydig cells, there is not correct differentiation of the internal and external genitalia
  • Sertoli cells produce AMH to inhibit paramesonephric/Mullerian duct development (female genital tract). In the late embryo, we see a huge increase in secretion (regression of Mullerian duct). Level of AMH remains high right to birth and through all of childhood period. May have a role in the onset of puberty (as it begins to decline, puberty comes in)
  • Leydig cells produce T. Elevates late in foetal period. Drops significantly at birth and only elevates again driving puberty (develops secondary sex characteristics)

Ovary

  • All the hormone secreting cells are present but there is no follicular development, so they don't secrete hormones (no surge in E and P to initiate menstrual cycle).
  • Different differentiation of the gonad

Placenta

  • Has many roles in development
  • In early placentagtion, the hCG it secretes supports the corpus luteum, to maintain the pregnancy (maintain functional layer of uterus). Secretions of corpus luteum supports decidualisation of the uterus layer
  • Placenta takes over role of supporting the functional layer of the uterus (key maintainer of pregnancy during foetal period).
  • Also produces chorionic somatotrophin and more. All these are called "human chorionic X" because they're from placenta. Last term
    • Thyrotrophin - stimulator of thyroid hormone secretion
    • Corticotrophin - similar to cortisol
    • Relaxin - makes joints more flexible for birthing
  • Surge of hCG up to 20 weeks, then plateaus
  • Secretion of steroid hormones, and also able to produce T

Other endocrine

  • From more recent research, that identified that many other tissue secrete hormones.
  • Don't need to know this.

Abnormalities

Because of different embryonic sources and because of migration, can get various abnormalities. Can also get functional abnormalities

Pineal

  • Hypoplasia - associated with retinal disease
  • Tumours can form - associated with

Pituitary

Thyroid

  • Trickle on event: lack of thyroid hormone causes lack of neurological development

Endocrine disruptors

  • There are those that mimic, block or interfere with development.