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Production, Regulation, and Action
Thyroid hormone
Histology of the Thyroid Gland
• The thyroid gland contains numerous follicles,
composed of epithelial follicle cells and colloid.
• Between follicles are clear parafollicular cells,
which produce calcitonin.
The Thyroid Gland – Histology
I
Why is Iodine Important in Thyroid Hormone
Production?
• Thyroid hormones are unique biological
molecules in that they incorporate iodine in their
structure.
• Thus, adequate iodine intake (diet, water) is
required for normal thyroid hormone production.
• Major sources of iodine:
- iodized salt
- iodated bread
- dairy products
- shellfish
• Minimum requirement: 75- 80 micrograms/day
Iodine Metabolism
• Dietary iodine is absorbed in the GI tract, then
taken up by the thyroid gland (or removed from
the body by the kidneys).
• The transport of iodide into follicular cells is
dependent upon a Na+/I- cotransport system.
• Iodide taken up by the thyroid gland is oxidized by
peroxide in the lumen of the follicle:
peroxidase
I- I+
• Oxidized iodine can then be used in production of
thyroid hormones.
Production of Thyroglobulin
 Pituitary produces TSH, which binds to follicle
cell receptors.
 The follicle cells of the thyroid produce
thyroglobulin.
 Thyroglobulin is a very large glycoprotein.
 Thyroglobulin is released into the colloid space,
where its tyrosine residues are iodinated by I+.
 This results in tyrosine residues which have one
or two iodines attached (monoiodotyrosine or
diiodotyrosine).
Thyroid Hormone Synthesis
Thyroid Hormones
 There are two biologically active thyroid
hormones:
- tetraiodothyronine (T4; usually called
thyroxine)
- triiodothyronine (T3)
 Derived from modification of tyrosine.
Differences between T4 and T3
 The thyroid secretes about 80 micro gm of T4, but
only 5 micro gm of T3 per day.
 However, T3 has a much greater biological activity
(about 10 X) than T4.
 An additional 25 microg/day of T3 is produced by
peripheral monodeiodination of T4.
T4
thyroid
I-
T3
TRIIODOTHYRONINE TETRAIODOTYROSINE
RAPID ACTION AND
DEGRADATION
SLOW TO RESPOND
10 x MORE RAPIDLY
BINDS TO RECEPTORS
SLOW BINDING
METABOLICALLY ACTIVE INACTIVE,CONVERTS TO
T3
DIFFERENCE IN ACTIONS OF T3 & T4
Transport of Thyroid Hormones
• Thyroid hormones are not very soluble in water (but
are lipid-soluble).
• Thus, they are found in the circulation associated with
binding proteins:
- Thyroid Hormone-Binding Globulin (~70% of
hormone)
- Pre-albumin (transthyretin), (~14%)
- Albumin (~15%)
• Less than 1% of thyroid hormone is found free in the
circulation.
• Only free and albumin-bound thyroid hormone is
biologically available to tissues.
One Major Advantage of this System
 The thyroid gland is capable of storing many
weeks worth of thyroid hormone (coupled to
thyroglobulin).
 If no iodine is available for this period,
thyroid hormone secretion will be
maintained.
Regulation of Thyroid Hormone Levels
 Thyroid hormone synthesis and secretion is
regulated by two main mechanisms:
- an “autoregulation” mechanism, which
reflects the available levels of iodine.
- regulation by the hypothalamus and
anterior pituitary.
Autoregulation of Thyroid Hormone
Production
 The rate of iodine uptake and incorporation
into thyroglobulin is influenced by the amount
of iodide available:
- low iodide levels increase iodine transport
into follicular cells
- high iodide levels decrease iodine transport
into follicular cells
Thus, there is negative feedback regulation of
iodide transport by iodide.
Neuroendocrine Regulation of Thyroid
Hormones: Role of TSH
 Thyroid-stimulating
hormone (TSH) is
produced by thyrotroph
cells of the anterior
pituitary.
 TSH is a glycoprotein
hormone composed of
two subunits:
- alpha subunit (common
to LH, FSH, TSH)
- TSH beta subunit, which
gives specificity of
receptor binding and
biological activity
a
LHb
FSHb TSHb
LH FSH TSH
Action of TSH on the Thyroid
 TSH acts on follicular cells of the thyroid.
- increases iodide transport into follicular cells
- increases production and iodination of
thyroglobulin
- increases endocytosis of colloid from lumen into
follicular cells
Na+
I-
thyroglobulinfollicle
cell
gene
I-
endocytosis
thyroglobulin
T3 T4
colloid droplet
I-I+
iodination
thyroglobulin
Na+ K+
ATP
Mechanism of Action of TSH
 TSH binds to a plasma membrane-bound, G
protein-coupled receptor on thyroid follicle cells.
 Specifically, it activates a Gs-coupled receptor,
resulting in increased cAMP production and PKA
activation.
TSH
Gsa
Adenylyl
Cyclase
ATP cyclic AMP
Protein kinase
A
Follicle cell
Thyroid Follicles
Influence of TRH on TSH Release
• Thyrotropin-releasing hormone (TRH) is a
hypothalamic releasing factor which travels
through the pituitary portal system to act on
anterior pituitary thyrotroph cells.
• TRH acts through G protein-coupled receptors,
activating the IP3 (Ca2+) and DAG (PKC) pathways
to cause increased production and release of TSH.
TRH phospholipase C
G protein-coupled
receptor
IP3 calcium
DAG PKC
calmodulin
• Thyroid hormones also inhibit TRH synthesis.
Negative Feedback Actions of Thyroid
Hormones on TSH Synthesis and Release
hypothalamus
TRH
TRH receptor
TSH synthesis
pituitary
T3/T4
+
-
-
-
TRH synthesis
Thyroid gland
follicle cell receptors
TSH binds
Thyroid hormone
Other Factors Regulating Thyroid Hormone
Levels
 Diet: a high carbohydrate diet increase T3 levels,
resulting in increased metabolic rate (diet-
induced thermogenesis).
 Low carbohydrate diets decrease T3 levels,
resulting in decreased metabolic rate.
 Cold Stress: increases T3 levels in other animals,
but not in humans.
 Any condition that increases body energy
requirements (e.g., pregnancy, prolonged cold)
stimulates hypothalamus  TRH  TSH (Pit)
conversion
 T4 can convert to T3 through deniodenation in
peripheral tissues as well as in the thyroid.
 (catalyzed by deiodinase).
Actions of Thyroid Hormones
 Thyroid hormones are essential for normal
growth of tissues, including the nervous
system.
 Lack of thyroid hormone during development
results in short stature and mental deficits
(cretinism).
 Thyroid hormone stimulates basal metabolic
rate.
Actions of Thyroid Hormone
 Required for GH and prolactin production
and secretion
 Required for GH action
 Increases intestinal glucose reabsorption
(glucose transporter)
 Increases mitochondrial oxidative
phosphorylation (ATP production)
 Increases activity of adrenal medulla
(sympathetic; glucose production)
 Induces enzyme synthesis
 Result: stimulation of growth of tissues and
increased metabolic rate. Increased heat
production (calorigenic effect)
Effects of Thyroid Hormone on Nutrient
Sources
• Effects on protein synthesis and degradation:
-increased protein synthesis at low thyroid
hormone levels (low metabolic rate; growth)
-increased protein degradation at high thyroid
hormone levels (high metabolic rate; energy)
• Effects on carbohydrates:
-low doses of thyroid hormone increase glycogen
synthesis (low metabolic rate; storage of energy)
- high doses increase glycogen breakdown (high
metabolic rate; glucose production)
Expression and Regulation of Thyroid
Hormone Receptors
 Thyroid hormone receptors are found in
many tissues of the body, but not in adult
brain, spleen, testes, uterus, and thyroid
gland itself.
 Thyroid hormone inhibits thyroid hormone
receptor expression (TRE on THR genes).
One Major Target Gene of T3: The Na+/K+
ATPase Pump
 Pumps sodium and potassium across cell
membranes to maintain resting membrane
potential
 Activity of the Na+/K+ pump uses up energy, in the
form of ATP
 About 1/3rd of all ATP in the body is used by the
Na+/K+ ATPase
 T3 increases the synthesis of Na+/K+ pumps,
markedly increasing ATP consumption.
 T3 also acts on mitochondria to increase ATP
synthesis
 The resulting increased metabolic rate increases
thermogenesis (heat production).
Thyroid hormones:
Key Points
• Held in storage
• Bound to mitochondria, thereby increasing ATP
production
• Bound to receptors activating genes that control energy
utilization
• Exert a calorigenic effect
Thyroid Hormone Actions which
Increase Oxygen Consumption
 Increase mitochondrial size, number and key enzymes
 Increase plasma membrane Na-K ATPase activity
 Decrease superoxide dismutase activity
 T3 /T4 can increase oxygen consumption, promote
metabolism and BMR(basal metabolic rate) ,↓utility.
Effects of Thyroid Hormones on the
Cardiovascular System
 Increase heart rate
 Increase force of cardiac contractions
 Increase stroke volume
 Increase Cardiac output
 Up-regulate catecholamine receptors
Effects of Thyroid Hormones on the
Respiratory System
 Increase resting respiratory rate
 Increase minute ventilation
 Increase ventilatory response to hypercapnia and
hypoxia
Effects of Thyroid Hormones on the
Renal System
 Increase blood flow
 Increase glomerular filtration rate
Effects of Thyroid Hormones on
Oxygen-Carrying Capacity
 Increase RBC mass
 Increase oxygen dissociation from hemoglobin
Effects of Thyroid Hormones on
Intermediary Metabolism
 Increase glucose absorption from the GI tract
 Increase carbohydrate, lipid and protein turnover
 Down-regulate insulin receptors
 Increase substrate availability
Effects Thyroid Hormones in
Growth and Tissue Development
 Increase growth and maturation of bone
 Increase tooth development and eruption
 Increase growth and maturation of
epidermis,hair follicles and nails
 Increase rate and force of skeletal muscle
contraction
 Inhibits synthesis and increases degradation of
mucopolysaccharides in subcutaneous tissue
Effects of Thyroid Hormones on the
Nervous System
 Critical for normal CNS neuronal development
 Enhances wakefulness and alertness
 Enhances memory and learning capacity
 Required for normal emotional tone
 Increase speed and amplitude of peripheral nerve
reflexes
Effects of Thyroid Hormones on the
Reproductive System
 Required for normal follicular development and
ovulation in the female
 Required for the normal maintenance of pregnancy
 Required for normal spermatogenesis in the male
 Calcium metabolism.
 Adrenal cortex.
Thyroid hormone
Thyroid Hormone Deficiency: Hypothyroidism
 Early onset: delayed/incomplete physical and
mental development
 Later onset (youth): Impaired physical growth
 Adult onset (myxedema) : gradual changes
occur. Tiredness, lethargy, decreased
metabolic rate, slowing of mental function and
motor activity, cold intolerance, weight gain,
goiter, hair loss, dry skin. Eventually may
result in coma.
 Many causes (insufficient iodine, lack of
thyroid gland, lack of hormone receptors, lack
of TH binding globulin….)
Hypothyroidism Symptoms
 Tiredness and weakness
 Dry skin
 Feeling cold
 Hair loss
 Difficulty in concentrating and poor memory
 Constipation
 Weight gain with poor
appetite
 Hoarse voice
 Menorrhagia, later
oligo and amenorrhoea
 Paresthesias
 Impaired hearing
Hypothyroidism Signs
 Dry skin, cool extremities
 Puffy face, hands and feet
 Delayed tendon reflex relaxation
 Carpal tunnel syndrome
 Bradycardia
 Diffuse alopecia
 Serous cavity effusions
Causes of Hypothyroidism
 Autoimmune
hypothyroidism
(Hashimoto’s, atrophic
thyroiditis)
 Iatrogenic (I123treatment,
thyroidectomy, external
irradiation of the neck)
 Drugs: iodine excess,
lithium, antithyroid drugs,
etc
 Iodine deficiency
 Infiltrative disorders of the
thyroid: amyloidosis,
sarcoidosis,haemochroma
tosis, scleroderma
Causes of Hyperthyroidism
Most common causes
 Graves disease
 Toxic multinodular
goiter
 Autonomously
functioning nodule
Rarer causes
 Thyroiditis or other causes
of destruction
 Thyrotoxicosis factitia
 Iodine excess (Jod-Basedow
phenomenon)
 Struma ovarii
 Secondary causes (TSH or
ßHCG)
Hyperthyroidism Symptoms
 Hyperactivity/ irritability/ dysphoria
 Heat intolerance and sweating
 Palpitations
 Fatigue and weakness
 Weight loss with increase of appetite
 Diarrhoea
 Polyuria
 Oligomenorrhoea, loss of libido
Hyperthyroidism Signs
 Tachycardia (AF)
 Tremor
 Goiter
 Warm moist skin
 Proximal muscle
weakness
 Lid retraction or lag
 Gynecomastia
Thyroid hormone
Thyroid hormone

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Thyroid hormone

  • 3. Histology of the Thyroid Gland • The thyroid gland contains numerous follicles, composed of epithelial follicle cells and colloid. • Between follicles are clear parafollicular cells, which produce calcitonin.
  • 4. The Thyroid Gland – Histology I
  • 5. Why is Iodine Important in Thyroid Hormone Production? • Thyroid hormones are unique biological molecules in that they incorporate iodine in their structure. • Thus, adequate iodine intake (diet, water) is required for normal thyroid hormone production. • Major sources of iodine: - iodized salt - iodated bread - dairy products - shellfish • Minimum requirement: 75- 80 micrograms/day
  • 6. Iodine Metabolism • Dietary iodine is absorbed in the GI tract, then taken up by the thyroid gland (or removed from the body by the kidneys). • The transport of iodide into follicular cells is dependent upon a Na+/I- cotransport system. • Iodide taken up by the thyroid gland is oxidized by peroxide in the lumen of the follicle: peroxidase I- I+ • Oxidized iodine can then be used in production of thyroid hormones.
  • 7. Production of Thyroglobulin  Pituitary produces TSH, which binds to follicle cell receptors.  The follicle cells of the thyroid produce thyroglobulin.  Thyroglobulin is a very large glycoprotein.  Thyroglobulin is released into the colloid space, where its tyrosine residues are iodinated by I+.  This results in tyrosine residues which have one or two iodines attached (monoiodotyrosine or diiodotyrosine).
  • 9. Thyroid Hormones  There are two biologically active thyroid hormones: - tetraiodothyronine (T4; usually called thyroxine) - triiodothyronine (T3)  Derived from modification of tyrosine.
  • 10. Differences between T4 and T3  The thyroid secretes about 80 micro gm of T4, but only 5 micro gm of T3 per day.  However, T3 has a much greater biological activity (about 10 X) than T4.  An additional 25 microg/day of T3 is produced by peripheral monodeiodination of T4. T4 thyroid I- T3
  • 11. TRIIODOTHYRONINE TETRAIODOTYROSINE RAPID ACTION AND DEGRADATION SLOW TO RESPOND 10 x MORE RAPIDLY BINDS TO RECEPTORS SLOW BINDING METABOLICALLY ACTIVE INACTIVE,CONVERTS TO T3 DIFFERENCE IN ACTIONS OF T3 & T4
  • 12. Transport of Thyroid Hormones • Thyroid hormones are not very soluble in water (but are lipid-soluble). • Thus, they are found in the circulation associated with binding proteins: - Thyroid Hormone-Binding Globulin (~70% of hormone) - Pre-albumin (transthyretin), (~14%) - Albumin (~15%) • Less than 1% of thyroid hormone is found free in the circulation. • Only free and albumin-bound thyroid hormone is biologically available to tissues.
  • 13. One Major Advantage of this System  The thyroid gland is capable of storing many weeks worth of thyroid hormone (coupled to thyroglobulin).  If no iodine is available for this period, thyroid hormone secretion will be maintained.
  • 14. Regulation of Thyroid Hormone Levels  Thyroid hormone synthesis and secretion is regulated by two main mechanisms: - an “autoregulation” mechanism, which reflects the available levels of iodine. - regulation by the hypothalamus and anterior pituitary.
  • 15. Autoregulation of Thyroid Hormone Production  The rate of iodine uptake and incorporation into thyroglobulin is influenced by the amount of iodide available: - low iodide levels increase iodine transport into follicular cells - high iodide levels decrease iodine transport into follicular cells Thus, there is negative feedback regulation of iodide transport by iodide.
  • 16. Neuroendocrine Regulation of Thyroid Hormones: Role of TSH  Thyroid-stimulating hormone (TSH) is produced by thyrotroph cells of the anterior pituitary.  TSH is a glycoprotein hormone composed of two subunits: - alpha subunit (common to LH, FSH, TSH) - TSH beta subunit, which gives specificity of receptor binding and biological activity a LHb FSHb TSHb LH FSH TSH
  • 17. Action of TSH on the Thyroid  TSH acts on follicular cells of the thyroid. - increases iodide transport into follicular cells - increases production and iodination of thyroglobulin - increases endocytosis of colloid from lumen into follicular cells Na+ I- thyroglobulinfollicle cell gene I- endocytosis thyroglobulin T3 T4 colloid droplet I-I+ iodination thyroglobulin Na+ K+ ATP
  • 18. Mechanism of Action of TSH  TSH binds to a plasma membrane-bound, G protein-coupled receptor on thyroid follicle cells.  Specifically, it activates a Gs-coupled receptor, resulting in increased cAMP production and PKA activation. TSH Gsa Adenylyl Cyclase ATP cyclic AMP Protein kinase A Follicle cell
  • 20. Influence of TRH on TSH Release • Thyrotropin-releasing hormone (TRH) is a hypothalamic releasing factor which travels through the pituitary portal system to act on anterior pituitary thyrotroph cells. • TRH acts through G protein-coupled receptors, activating the IP3 (Ca2+) and DAG (PKC) pathways to cause increased production and release of TSH. TRH phospholipase C G protein-coupled receptor IP3 calcium DAG PKC calmodulin • Thyroid hormones also inhibit TRH synthesis.
  • 21. Negative Feedback Actions of Thyroid Hormones on TSH Synthesis and Release hypothalamus TRH TRH receptor TSH synthesis pituitary T3/T4 + - - - TRH synthesis Thyroid gland follicle cell receptors TSH binds
  • 23. Other Factors Regulating Thyroid Hormone Levels  Diet: a high carbohydrate diet increase T3 levels, resulting in increased metabolic rate (diet- induced thermogenesis).  Low carbohydrate diets decrease T3 levels, resulting in decreased metabolic rate.  Cold Stress: increases T3 levels in other animals, but not in humans.  Any condition that increases body energy requirements (e.g., pregnancy, prolonged cold) stimulates hypothalamus  TRH  TSH (Pit)
  • 24. conversion  T4 can convert to T3 through deniodenation in peripheral tissues as well as in the thyroid.  (catalyzed by deiodinase).
  • 25. Actions of Thyroid Hormones  Thyroid hormones are essential for normal growth of tissues, including the nervous system.  Lack of thyroid hormone during development results in short stature and mental deficits (cretinism).  Thyroid hormone stimulates basal metabolic rate.
  • 26. Actions of Thyroid Hormone  Required for GH and prolactin production and secretion  Required for GH action  Increases intestinal glucose reabsorption (glucose transporter)  Increases mitochondrial oxidative phosphorylation (ATP production)  Increases activity of adrenal medulla (sympathetic; glucose production)  Induces enzyme synthesis  Result: stimulation of growth of tissues and increased metabolic rate. Increased heat production (calorigenic effect)
  • 27. Effects of Thyroid Hormone on Nutrient Sources • Effects on protein synthesis and degradation: -increased protein synthesis at low thyroid hormone levels (low metabolic rate; growth) -increased protein degradation at high thyroid hormone levels (high metabolic rate; energy) • Effects on carbohydrates: -low doses of thyroid hormone increase glycogen synthesis (low metabolic rate; storage of energy) - high doses increase glycogen breakdown (high metabolic rate; glucose production)
  • 28. Expression and Regulation of Thyroid Hormone Receptors  Thyroid hormone receptors are found in many tissues of the body, but not in adult brain, spleen, testes, uterus, and thyroid gland itself.  Thyroid hormone inhibits thyroid hormone receptor expression (TRE on THR genes).
  • 29. One Major Target Gene of T3: The Na+/K+ ATPase Pump  Pumps sodium and potassium across cell membranes to maintain resting membrane potential  Activity of the Na+/K+ pump uses up energy, in the form of ATP  About 1/3rd of all ATP in the body is used by the Na+/K+ ATPase  T3 increases the synthesis of Na+/K+ pumps, markedly increasing ATP consumption.  T3 also acts on mitochondria to increase ATP synthesis  The resulting increased metabolic rate increases thermogenesis (heat production).
  • 30. Thyroid hormones: Key Points • Held in storage • Bound to mitochondria, thereby increasing ATP production • Bound to receptors activating genes that control energy utilization • Exert a calorigenic effect
  • 31. Thyroid Hormone Actions which Increase Oxygen Consumption  Increase mitochondrial size, number and key enzymes  Increase plasma membrane Na-K ATPase activity  Decrease superoxide dismutase activity  T3 /T4 can increase oxygen consumption, promote metabolism and BMR(basal metabolic rate) ,↓utility.
  • 32. Effects of Thyroid Hormones on the Cardiovascular System  Increase heart rate  Increase force of cardiac contractions  Increase stroke volume  Increase Cardiac output  Up-regulate catecholamine receptors
  • 33. Effects of Thyroid Hormones on the Respiratory System  Increase resting respiratory rate  Increase minute ventilation  Increase ventilatory response to hypercapnia and hypoxia
  • 34. Effects of Thyroid Hormones on the Renal System  Increase blood flow  Increase glomerular filtration rate
  • 35. Effects of Thyroid Hormones on Oxygen-Carrying Capacity  Increase RBC mass  Increase oxygen dissociation from hemoglobin
  • 36. Effects of Thyroid Hormones on Intermediary Metabolism  Increase glucose absorption from the GI tract  Increase carbohydrate, lipid and protein turnover  Down-regulate insulin receptors  Increase substrate availability
  • 37. Effects Thyroid Hormones in Growth and Tissue Development  Increase growth and maturation of bone  Increase tooth development and eruption  Increase growth and maturation of epidermis,hair follicles and nails  Increase rate and force of skeletal muscle contraction  Inhibits synthesis and increases degradation of mucopolysaccharides in subcutaneous tissue
  • 38. Effects of Thyroid Hormones on the Nervous System  Critical for normal CNS neuronal development  Enhances wakefulness and alertness  Enhances memory and learning capacity  Required for normal emotional tone  Increase speed and amplitude of peripheral nerve reflexes
  • 39. Effects of Thyroid Hormones on the Reproductive System  Required for normal follicular development and ovulation in the female  Required for the normal maintenance of pregnancy  Required for normal spermatogenesis in the male
  • 40.  Calcium metabolism.  Adrenal cortex.
  • 42. Thyroid Hormone Deficiency: Hypothyroidism  Early onset: delayed/incomplete physical and mental development  Later onset (youth): Impaired physical growth  Adult onset (myxedema) : gradual changes occur. Tiredness, lethargy, decreased metabolic rate, slowing of mental function and motor activity, cold intolerance, weight gain, goiter, hair loss, dry skin. Eventually may result in coma.  Many causes (insufficient iodine, lack of thyroid gland, lack of hormone receptors, lack of TH binding globulin….)
  • 43. Hypothyroidism Symptoms  Tiredness and weakness  Dry skin  Feeling cold  Hair loss  Difficulty in concentrating and poor memory  Constipation  Weight gain with poor appetite  Hoarse voice  Menorrhagia, later oligo and amenorrhoea  Paresthesias  Impaired hearing
  • 44. Hypothyroidism Signs  Dry skin, cool extremities  Puffy face, hands and feet  Delayed tendon reflex relaxation  Carpal tunnel syndrome  Bradycardia  Diffuse alopecia  Serous cavity effusions
  • 45. Causes of Hypothyroidism  Autoimmune hypothyroidism (Hashimoto’s, atrophic thyroiditis)  Iatrogenic (I123treatment, thyroidectomy, external irradiation of the neck)  Drugs: iodine excess, lithium, antithyroid drugs, etc  Iodine deficiency  Infiltrative disorders of the thyroid: amyloidosis, sarcoidosis,haemochroma tosis, scleroderma
  • 46. Causes of Hyperthyroidism Most common causes  Graves disease  Toxic multinodular goiter  Autonomously functioning nodule Rarer causes  Thyroiditis or other causes of destruction  Thyrotoxicosis factitia  Iodine excess (Jod-Basedow phenomenon)  Struma ovarii  Secondary causes (TSH or ßHCG)
  • 47. Hyperthyroidism Symptoms  Hyperactivity/ irritability/ dysphoria  Heat intolerance and sweating  Palpitations  Fatigue and weakness  Weight loss with increase of appetite  Diarrhoea  Polyuria  Oligomenorrhoea, loss of libido
  • 48. Hyperthyroidism Signs  Tachycardia (AF)  Tremor  Goiter  Warm moist skin  Proximal muscle weakness  Lid retraction or lag  Gynecomastia