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Week 5 Lecture 13: Endocrine System (Thyroid gland (Synthesis and…
Week 5 Lecture 13: Endocrine System
Posterior pituitary
Releases
neurohormones
Any hormone produce and released by
neuroendocrine cells
into the blood
These are neurons that secrete hormones
Process
1.
Hypothalamic
neurons
produce
the neurohormones
ADH
and
oxytocin
in the cell body
2.
The neurohormones are transported to the posterior pituitary
3.
ADH and oxytocin are released into the interstitial fluid of the posterior pituitary, then into the
capillaries
, for transport to the rest of the body
Capillary networks of the pituitary gland
Different in both anterior and posterior pituitary
Anterior pituitary
Axon terminals
do not
end up in the anterior pituitary
The terminals secrete
releasing factors
(neurohormones from the hypothalamus) in a hypothalamic capillary network, which travel through
portal vessels
into the anterior pituitary
The neurohormones stimulate or inhibit the release of hormones from the anterior pituitary
cells
, into the veins, then into the systemic circuit
NB: These are NOT neurohormones because the AP hormones are NOT released by neurons :red_cross: :warning:
Posterior pituitary
Axon terminals end up in the interstitial fluid of the posterior pituitary
The neurohormones in the interstitial fluid make their way into the
posterior capillaries
then into
veins
for transport out into the systemic circuit
Anterior pituitary
Regulated by the
hypothalamus
Feedback loops
External or internal stimuli (e.g. stress or temperature)...
:check:
Causes
hypothalamus
to secrete
releasing hormones
#
:check:
Causes the
anterior pituitary
to release their hormones
#
:check:
1 more item...
:no_entry:
#
:no_entry: (inhibits hypothalamus)
:check: for stimulation (positive feedback)
:no_entry: for inhibition (negative feedback)
How does the signal tell the hypothalamus and pituitary that no more hormone is needed?
Receptors
are present on the hypothalamus and pituitary, specific to specific hormones
Thyroid gland
Produces the hormone
thyroxine
(T3)
Most cells have
receptors
for thyroxine in the
nucleus
NOT in cytosol, so no need for chaperone molecules :red_cross:
Thyroxine goes straight through the nuclear pores – it is
lipid soluble
(lipophilic)
Thyroxine signals to the hypothalamus to signal the pituitary to release thyrotropin stimulating hormone (TSH)
TSH signals the thyroid gland to release thyroxine
Thyroxine is released via the activation of transcription of enzymes involved in energy metabolic pathways
This
elevates
the metabolic rates of most cells
e.g. from exposure to cold
Functions
Regulates
the
metabolic rate
of most cells in the body
Crucial for normal development and growth
Too little thyroxine from
lack of iodine
in pregnant women retards foetal/child growth
Leads to a condition called
cretinism
Regulation
Feedback loops
External or internal stimuli (e.g. stress or temperature)...
:check:
Hypothalamus
#
#
:check:
Production of thyrotropin-releasing hormone (TRH)
1 more item...
:no_entry:
Anatomy
Thyroid gland is
below
the voice box (no vibration felt)
Made up of two glands
Complications/diseases
Both hypothyroidism and hyperthyroidism can cause a
goiter
to form (an enlarged thyroid)
Hypothyroidism
Can cause formation of a
goiter
Enlarged thyroid
Results from constant
stimulation
of
cell division
The need to have more follicle (cuboidal epithelial) cells for
thyroglobulin to pick up iodine
(iodinate)
Very
low
levels of thyroxine
Symptoms
Weakness
Lethargy
Weight
gain
Blurry eyesight
Dry
skin
Irritability
Memory loss
Causes
Low dietary iodine
Follicle cells fail to make thyroxine
Autoimmune disease
Hashimoto's disease
Pituitary disease
Thyroiditis
Feedback loop
Hypothalamus
:check:
Production of thyrotropin-releasing hormone
:check:
1 more item...
Treatment
Levothyroxine
Daily pure synthetic form of T4
This will get converted to T3
Supplementation of iodine
The WHO has mandated governments in all countries (by legislation) to make
iodised salt
an important part of the diet
In
Australia
, this is a requirement in ALL
processed foods
Hyperthyroidism
(Graves disease)
Can
also
cause formation of a
goiter
Enlarged thyroid
Results from constant
stimulation
of
cell division
The need to have more follicle (cuboidal epithelial) cells to
create thyroxine
Very
high
levels of thyroxine
Symptoms
Weakness
Lethargy
Weight
loss
Blurry eyesight
Moist
skin
Insomnia
Palpitations
Usually associated with an abnormal heart rhythm (
arrhythmia
)
Bulging eyes
Nervousness
An
autoimmune
disease
Disease cause by antibodies or lymphocytes produced against substances naturally present in the body
Feedback loop
Hypothalamus
:check:
Production of thyrotropin-releasing hormone (TRH)
:check:
1 more item...
Treatment
Inhibits the enzyme thyroperoxidase to prevent iodination of thyroglobulin
Methimazole
Neomercazole
Propylthiouracil
Histology
Follicle
Each lined by
cuboidal epithelial cells
– i.e. follicular cells
Thyroxine is synthesised in each of these follicular cells
Follicular lumen
A cavity within the follicle, surrounded by
follicular cells
(cuboidal epithelial cells) and filled with
colloid
, a concentrated solution of thyroglobulin
Synthesis and secretion of thyroxine
1.
A follicle cell takes up
iodine
from the blood
Supplemented by our
diet
(e.g. in salt)
2.
The follicle cell synthesises
thyroglobulin
(a polymer) from
tyrosine
, a non-essential amino acid
3.
Thyroglobulin and
iodine
are secreted into the follicular lumen
Thyroglobulin is then
iodinated
(add iodine)
4.
Iodinated thyroglobulin is taken up by a follicle cell by
endocytosis
5.
Enzymes in the vesicle
digest
thyroglobulin into T3 and T4
Triiodothyronine (T3)
The
active hormone
Three iodine molecules attached
Tetraiodothyronine (T4) – otherwise known as
thyroxine
The
precursor
When it reaches the target cell, it will
convert
to T3
Four iodine molecules attached
Since T3 and T4 are in a vesicle, they are
water soluble
, i.e.
lipophobic
6.
T3 and T4 are both secreted via
exocytosis
into the
blood
to target cells