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Endocrine glands
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Hormones are chemical messengers secreted into the blood; can be
o Protein hormones (e
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TSH, GH) acting on a cell membrane
 Stimulate internal signalling cascades, thus a quick reaction
o Steroid hormones (e
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oestrogen and testosterone) can diffuse
directly through the membrane and act on intracellular receptors
 Typically stimulate transcription/translation activity, so slower
o Tyrosine derivatives; can act like protein hormones on a cell receptor
(e
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catecholamines) or like a steroid, diffusing through cell
membrane (e
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T3/T4)

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Exocrine glands secrete product into an epithelial duct
Endocrine gland cells secrete hormones into vasculature
o Typically aggregate as cord/follicles
o Some organs contain endocrine cells e
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heart, kidneys, gonads
Some endocrine cells produce hormones that act locally
o Paracrine (local distribution in interstitial fluid or capillaries)
o Juxtacrine (hormone remains on cell surface/ECM)
o Autocrine
Hormones
o Can be hydrophilic (proteins, glycoproteins, peptides, modified amino
acids) that bind cell surface receptors
o Can be hydrophobic (steroid/thyroid hormones) that circulate on
transport proteins and diffuse directly through the cell membrane
o Hormones acting on a cell surface receptor often bring about changes
quicker than steroid hormones (involves transcription and translation)

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Taken from Mescher, Junqueira’s Basic Histology: text and Atlas, Twelfth Edition
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Blood supply to the pituitary gland (hypothalamo-hypophyseal portal system)
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Superior hypophyseal arteries (branch of internal carotid artery) supply the
median eminence and the infundibular stalk
o Primary capillary network around the infundibular stalk; secondary
capillary network in the adenohypophysis; capillaries fenestrated
Inferior hypophyseal arteries supply the neurohypophysis (plus a bit of stalk)
Neuropeptides from the median eminence are taken to the
adenohypophysis – stimulate/inhibit endocrine hormone release
Hormone release at three sites
o Peptide hormones synthesised in supraoptic and paraventricular nuclei
of the hypothalamus release into the capillaries at the pars nervosa
o Peptides produced by the dorsal medial, ventral medial and
infundibular nuclei of the hypothalamus release in the primary
capillary plexus
o Proteins and glycoproteins synthesised by the pars distalis released into
hypophyseal vein

Taken from Mescher, Junqueira’s Basic Histology: Text and Atlas, Twelfth Edition
...
Include somatotrophic (produce GH),
mammotropic (prolactin), gonadotrophic (produce FSH, LH),
corticotrophic (ACTH), and thyrotrophic (TSH) cells
o FLAT GP to remember all the hormones; also FLAT are basophilic, and
act via another endocrine organ to bring effects (e
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ovaries, adrenal
gland, thyroid), while GP are acidophobic, and act directly on target
(e
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GH on muscle and bone, prolactin on mammary glands)
o Chemophobes: few granules, weakly stained

Taken from Mescher, Junqueira’s Basic Histology: Text and Atlas, Twelfth Edition
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Neurohypophysis
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No secretory cells; contains the unmyelinated axons of secretory neurons that
are located in the supraoptic and paraventricular nuclei of the hypothalamus
Also contains loads of pituicytes (branched glial cells, similar to astrocytes)
Secretory neurons synthesise vasopressin/ADH and oxytocin; accumulate in
neurosecretory/Herring bodies
o Vasopressin/ADH and oxytocin are bound to carrier proteins
neurophysin I and neurophysin II, respectively

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Supraoptic nuclei – vasopressin/ADH secretion; paraventricular nuclei –
oxytocin
Osmoreceptors in the hypothalamus detect increased tonicity of blood;
stimulate supraoptic neurons to produce ADH
o Effect is to increase permeability of kidney collecting ducts to water;
more water reabsorbed back into the blood; osmotic balance
returned
Clinical notes

Insulin-dependent diabetes/diabetes insipidus (juvenile)
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Don’t produce vasopressin/ADH – no upregulation of aquaporins in
the distal convoluted tubule of the kidney, thus Na+ is not reabsorbed
into the blood – can’t retain water
Constantly thirsty, urinate frequently
Can be caused by head injury, pituitary tumour
Can give vasopressin as a drug to treat

Pituitary tumour
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Optic chiasm located just above the pituitary gland – therefore
pituitary tumours, among other symptoms, can cause blurred vision or
loss of peripheral vision
Parasphenoidal surgery for removal of parathyroid tumour (via nose)

Postpartum-hypopituitarism
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Block in blood vessels above pituitary gland (ischemic necrosis); no
hormones produced
Known as Sheehan’s syndrome
Agalactorrhea, amenorrhea, hypothyroidism (tiredness, intolerant to
cold, weight gain, hair loss), slowed heart rate, low blood pressure,
adrenal insufficiency (fatigue, weight loss hypoglycaemia,
hyponatremia)

Gigantism and acromegaly
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Excessive GH as a child results in gigantism
o Growth plates not fully formed so bones can grow; grow to
extremely tall height, long limbs
Excessive GH as an adult – acromegaly
o Growth plates have fused so bones cannot grow further –
somatotrophic, so get thickened features
Treat both with surgery or GH-antagonist

Adrenal (suprarenal) glands
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Paired, located on superior poles of the kidneys, embedded in perirenal
adipose tissue
Surrounded by dense connective tissue capsule
Glands consist of peripheral yellow layer (adrenal cortex) and reddish-brown
central layer (adrenal medulla)
o Medulla is neurodermal origin, cortex is mesenchymal origin
All adrenal hormones are made from cholesterol; stimulated by ACTH

Blood supply of the adrenal glands
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Supplied by several arteries
o Capsule supplied by the cortical arterioles
o Medulla supplied by the medullary arterioles
Capillary and sinusoidal endothelium is highly fenestrated
Capillaries from the cortex and medulla form the medullary veins, which join
to leave the gland as the adrenal/suprarenal vein

Taken from Mescher, Junqueira’s Basic Histology: Text and Atlas, Twelfth Edition
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Lots of SER,
containing enzymes for steroid hormone synthesis
Mitochondria are also involved in steroid hormone synthesis – more spherical
in adrenal cortex cells, with tubular cristae
Product is not stored in granules; steroids are low MW and lipid-soluble so
diffuse freely through plasma membrane

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Concentric zones within the adrenal cortex; gets better as goes in - from salty,
to sweet to sex!
o Zona glomerulosa: located immediately inside connective tissue;
closely packed cords of pyramidal/columnar cells, lots of capillaries
 Produces mineralcorticoids
 e
...
aldosterone regulates salt balance by stimulates Na+
reabsorbtion in the kidney, in place of K+
 Stimulated by ACTH
o Zona fasiculata: middle zone, comprises long cords of large polyhedral
cells, separated by fenestrated sinusoidal capillaries
 Cells filled with lipid droplets; secrete glucocorticoids
 e
...
cortisol (carbohydrate metabolism; stimulates production of
glucose from amino acids/fatty acids (gluconeogenesis) and
glucose conversion to glycogen in the liver
 Diurnal variation
 Glucocorticoid secretion stimulated by ACTH from anterior
pituitary; feedback via pituitary and hypothalamus
o Zona reticularis: contacts the adrenal medulla; smaller cells forming
irregular cords with wide capillaries
 Produces DHEA, a weak androgen that is converted to
testosterone in target tissues
 DHEA secretion stimulated by ACTH; feedback via regulation of
pituitary and hypothalamus

Foetal adrenal cortex
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Larger at birth than in adult (provisional cortex) – comprises 80% of the gland
at this stage
o Located below the thin permanent cortex and above an
underdeveloped medulla
Mostly consists of large, steroid-secreting cells under pituitary control
o Mainly secretes DHEA – converted in the placenta to estrogens and
androgens
Important part of foetoplacental unit – unclear true function, but affects both
endocrine systems during pregnancy
After birth, the provisional cortex involutes, permanent cortex develops three
layers and medulla develops

Clinical note
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Disorders of the adrenal cortex can be hypofunctional or
hyperfunctional
Patients treated with corticoids for a prolonged period of time shouldn’t
suddenly stop taking them; secretion of ACTH is inhibited, so the cortex
will not produce corticoids, causing severe drops in Na+/K+

Cushing syndrome
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Tumour of adrenal cortex - increased production of glucocorticoids
Usually due to a pituitary adenoma (>90%); excessive ACTH
Precocious puberty in boys, and hirsuitism and virilisation in girls

Conn syndrome
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Tumour producing excessive aldosterone

Addison disease
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Destruction of adrenal cortex; adrenocortical insufficiency
Failed secretion of glucocorticoids and mineralocorticoids

Carcinomas of the adrenal cortex
Very rare; 90% produce steroids associated with endocrine glands
Adrenal medulla
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Innervated, developed from neural tissue – direct from spinal cord, synapse
directly on the Chromaffin cells
Large cells arranged in cords, supported by reticular fibre network
Sinusoidal capillaries between each cord, parasympathetic ganglion cells
The parenchymal cells are chromaffin cells; these are modified sympathetic
postganglionic neurons (no axons or dendrites, specialised in secretion)
Chromaffin cells contain electron-dense granules containing catecholamines
– either epinephrine or norepinephine
Catecholamines within the granules are bound to proteins called
chromatogranins

Taken from Mescher, Junqueira’s Basic Histology: Text and Atlas, Twelfth Edition
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Medical application
Insulin-independent diabetes/diabetes mellitus (types I and II)
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Type I - immune destruction of B cells
o Hyperglycaemic (lack of insulin)
o Get diabetic ketoacidosis; muscles break down
Type II - failure of target cells to respond to insulin, associated
with obesity

Islet cell tumours
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May produce insulin, glucagon, somatostatin, pancreatic
polypeptide
Can produce more than one hormone in excess, leading to
complicated clinical symptoms

Diffuse neuroendocrine system
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Dispersed hormone-secreting cells with commonalities to neurons, found
within the epithelium of various organs of the body e
...
enterochromaffin
cells of pancreatic islets, gut mucosa, respiratory mucosa
o Also known as gastroenteropancreatic (GEP) endocrine cells

Thyroid gland
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Develops from the ectoderm, two lobes connected by an isthmus
Cervical region, anterior to larynx
Synthesises thyroid hormones thyroxine (T4), tri-iodothyronine (T3), needed
for growth, metabolic rate, cell differentiation
Surrounded by a fibrous capsule, with septa separating the gland into
lobules and carrying blood vessels, nerves and lymphatics
Parenchyma consists of rounded epithelial structures called thyroid follicles
o Follicles separated by sparse reticular connective tissue
Follicles comprise simple epithelium (range from squamous to low
cuboidal); rich in RER and secretory granules containing colloidal material
Central lumen of the follicle is filled with colloid, a gelatinous substance;
contains thyroglobulin, a large glycoprotein that is the precursor of the
active thyroid hormones
Unusual secretion – only endocrine gland where large amount of product
is stored
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Control of thyroid function
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TSH secreted by anterior pituitary; TSH receptors on follicular cells; stimulates
thyroid hormone synthesis and release
Thyroid hormones inhibit TSH – negative feedback loop

Storage and release of thyroid hormone
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Exocrine and endocrine phases
Thyroglobulin produced by epithelial cells of the follicle; released from large
vesicles at apical surface into the lumen
Follicular cells uptake circulating iodide by the Na/I symporter/cotransporter
on basal membrane; increased concentration of iodide in these cells
Iodide transferred to follicular lumen via anion transport protein pendrin;
oxidised to active iodine by membrane-bound thyroid peroxidise
Tyrosine residues of thyroglobulin are iodinated covalently with iodine; forms
T3 or T4 (still attached to thyroglobulin)
In the endocrine phase, the follicular cells take up the iodinated thyroglobulin
via endocytosis or pinocytosis; endocytic vesicles fuse with lysosomes,
thyroglobulin is degraded, and T3 and T4 are released, cross cell membrane
into circulation (bind carrier proteins)
o T4 is the pro-hormone (always converted to T3)
o T3 is more active, but less abundant than T4

Clinical note
Iodine deficiency goitre
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Low iodine diet prevents thyroid hormone synthesis, causing increased
TSH production and inc growth of the thyroid gland

Foetal hypothyroidism
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Can cause cretinism (retarded physical and/or metal development)

Adult hypothyroidism
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From disease of thyroid gland (e
...
autoimmune disease, Hashimoto
disease, impairing function) or secondary due to
pituitary/hypothalamic failure
Cold intolerance, weight gain, lose outer third of eyebrow, hair
thinning, lethargy constipation, mental fog

Hyperthyroidism
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Graves disease – autoimmune response, Abs to TSH receptors
Inflammation and growth of the extraocular adipose tissue – bulging
eyes (exophthalmos; antibodies cross-react on optic nuclei), also
decreased body weight, tachycardia, heat intolerance

Parathyroid glands
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Four small glands located behind the thyroid gland (but not attached),
embedded in the thyroid gland capsule
o Some people can have up to eight
Same blood supply as the thyroid
Two types of cells present
o Chief (principal) cells: cytoplasm filled with granules of parathyroid
hormone (PTH), which regulates Ca2+ levels
o Oxyphil cells: smaller, clustered cells, abnormal shaped mitochondria
PTH targets osteoblasts, which respond by producing osteoclast-stimulating
factor (RANK-L) to increase the number and activity of osteoclasts – promotes
resorption of Ca2+ into the blood (negative feedback to reduce PTH)
o Also stimulates Vit D synthesis in GI tract, which promotes Ca2+
absorption
So PTH and calcitonin have opposing roles in regulating Ca2+ levels
PTH also targets renal tubule cells to increase Ca2+ reabsorption

Clinical note
Hyperparathyroidism
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Can be primary (parathyroid tumour) or secondary (low Ca2+ due
to e
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diet; PTH continually released to try and raise levels)
Blood phosphate decreased, blood Ca2+ increased
Pathological deposits of Ca2+ on organs, including kidney and
arteries
Get bones (osteoporosis), moans (depression), groans (aches and
pains), stones (kidney stones)
Osteitis fibrosa cystica - bones less stress-resistant, prone to fractures

Hypoparathyroidism
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Can be due to e
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accidental removal during surgery
Blood phosphate increased, blood Ca2+ decreased
Bones denser and more mineralised
Spastic contractions of skeletal muscles and convulsions (tetany);
exaggerated excitability of the nervous system due to low Ca2+
Treat with Ca2+ salts and vit D to promote Ca2+ uptake in the gut

Paraneoplastic syndrome
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Hormone mimics produced by cancer e
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breast cancer, causing
remodelling of bone to promote colonisation of bone by metastasis

Pineal gland
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Regulates daily rhythm of bodily activities
Small, pine cone shaped organ in the brain
Pinealiocytes contain secretory vesicles, lots of mitochondria
o Produce melatonin
Interstitial glial cells resemble astrocytes
Presence of variously sized concentrations of calcium and magnesium salts
called corpora arenacea – precipitates around extracellular protein deposits
Melatonin release is promoted by darkness and inhibited in light; diurnal
fluctuations in blood melatonin induces rhythmic changes in activity of the
hypothalamus, pituitary gland and other endocrine tissues
o Circadian rhythm
Light and dark detected in the retina and transmitted via neurons to the
pineal gland

Reference
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Junqueira’s Basic Histology: Text and Atlas
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