M.Sc.

ZOOLOGY 2nd SEMESTER (2025)

ASSIGNMENT

PAPER – MAMMALIAN
ENDOCRINOLOGY
TOPIC-Thyroid Gland

SUBMITTED BY:- SUBMITTED

TO:-
AANCHAL DEPARTMENT OF
ROLL NO.- 2240310440001 ZOOLOGY
DR. ANUHARIKA
CHAUHAN
 Index
1. Introduction to Thyroid Gland
2. Detailed Structure of Thyroid Gland
3. Biosynthesis of Thyroid Hormones
4. Control of Secretion of Thyroid Hormones
5. Transport of Thyroid Hormones
6. Denaturation of Thyroid Hormones
7. Physiological Roles of Thyroid Hormones
8. Morphological Consequences of Excess Thyroid Hormones
9. Morphological Consequences of Deficiency of Thyroid Hormones
10.Chemical Consequences of Excess Thyroid Hormones
11.Chemical Consequences of Deficiency of Thyroid Hormones
12.Disorders Associated with Thyroid Gland
13.Diagnostic Techniques for Thyroid Disorders
14.Therapeutic Approaches to Thyroid Disorders
15.References
1. Introduction to Thyroid Gland

• Endocrine Gland: The thyroid is a vital endocrine gland located in the neck, just
below the larynx. It plays a pivotal role in regulating metabolic processes in the
body by releasing thyroid hormones.
• Hormones Produced: The thyroid primarily produces two major hormones:
thyroxine (T4) and triiodothyronine (T3). These hormones are critical for the
regulation of metabolism, energy production, and general bodily functions.
• Metabolic Regulation: Thyroid hormones control the rate at which cells convert
nutrients into energy, thus directly affecting body temperature, energy levels, and
heart rate.
• Growth and Development: In children, thyroid hormones are essential for proper
growth and development, including brain maturation.
• Iodine Requirement: The thyroid uses iodine from the diet to produce thyroid
hormones. Iodine deficiency can result in thyroid dysfunction.
• Thyroid Dysfunction: Disorders such as hypothyroidism (underactive thyroid)
and hyperthyroidism (overactive thyroid) are commonly associated with the
thyroid gland, affecting metabolism and overall health.
• Location and Shape: The thyroid is located in the lower part of the neck, shaped
like a butterfly, with two lobes connected by an isthmus.
• Thyroid and Pituitary Gland Interaction: The secretion of thyroid hormones is
regulated by the hypothalamus and pituitary gland through a feedback loop
involving TSH (thyroid-stimulating hormone).
• Enzyme Activity: Thyroid hormones also influence the activity of enzymes
involved in various biochemical pathways like protein synthesis and glycolysis.
• Body Temperature Regulation: These hormones are involved in regulating the
body’s heat production and maintaining thermal homeostasis.
• Impact on Lipid Metabolism: Thyroid hormones increase lipid catabolism and
help maintain cholesterol levels in the body, influencing cardiovascular health.
• Neurodevelopment: Thyroid hormones are essential for the proper development
of the brain, particularly during fetal and early childhood stages.
• Immune System Effects: Thyroid dysfunction can affect the immune system,
potentially leading to autoimmune thyroid diseases like Hashimoto's thyroiditis
and Graves' disease.
2. Detailed Structure of Thyroid Gland

• Anatomical Location: The thyroid is situated in the anterior part of the neck, just
below the larynx and in front of the trachea. It consists of two lobes, one on either
side of the windpipe, connected by a narrow isthmus.
• Thyroid Follicles: The thyroid gland is primarily made of spherical structures
known as thyroid follicles. These follicles are filled with a colloid substance,
which is crucial for hormone production and storage.
• Thyroid Follicular Cells: The walls of the follicles are lined with thyroid
follicular cells. These cells are responsible for producing thyroid hormones,
namely T4 and T3, from iodinated tyrosine residues in the colloid.
• Parafollicular Cells (C-cells): Located between the follicles, C-cells secrete
calcitonin, a hormone that plays a role in regulating calcium levels in the body.
• Capillaries and Blood Flow: The thyroid is richly supplied with blood vessels,
which bring iodine and other nutrients necessary for hormone production. The
blood supply is primarily through the superior and inferior thyroid arteries.
• Thyroid Capsule: The gland is enclosed by a fibrous capsule that provides
structural integrity and separates it from surrounding tissues.
• Lymphatic Drainage: The thyroid has its own network of lymphatic vessels that
drain into nearby lymph nodes, playing a role in immune surveillance.
• Cellular Activity: The follicular cells in the thyroid are responsible for the uptake
of iodine, which is essential for thyroid hormone synthesis. They actively
transport iodine from the bloodstream into the colloid.
• Secretion Pathway: Once synthesized, thyroid hormones are stored in the colloid
until the body signals the need for their release, typically through a negative
feedback loop involving TSH.
• Thyroid Hormone Synthesis: The thyroid uses iodine, along with tyrosine, to
synthesize thyroid hormones within the colloid. These hormones are stored in the
gland and released as needed.
• Size and Variation: The size and shape of the thyroid can vary between
individuals. In some cases, such as iodine deficiency, the gland can become
enlarged, leading to a condition called goiter.
• Thyroid Lymphatic System: The thyroid's lymphatic system helps in draining
excess fluids and monitoring the presence of potential pathogens or abnormal
cells.
• Structural Adaptation to Function: The structure of the thyroid is designed to
maximize iodine uptake and hormone production, ensuring that the body's
metabolic needs are met efficiently.
• Intercellular Communication: Follicular cells communicate with one another
through gap junctions, ensuring synchronized hormone production and release.
• Hormone Storage: The colloid within the thyroid follicles serves as a storage
medium for thyroid hormones in their precursor form until they are required by
the body.
3. Biosynthesis of Thyroid Hormones

• Iodine Uptake: The process begins with the active transport of iodine ions from
the bloodstream into the thyroid follicular cells via the sodium-iodine symporter
(NIS).
• Oxidation of Iodine: Once inside the follicular cells, iodine is transported into
the colloid, where it is oxidized by the enzyme thyroid peroxidase (TPO).
• Iodination of Tyrosine: The oxidized iodine is then bound to tyrosine residues in
thyroglobulin, a large protein synthesized by follicular cells. This forms
monoiodotyrosine (MIT) and diiodotyrosine (DIT).
• Coupling of MIT and DIT: Two molecules of DIT or one molecule of MIT and
DIT are coupled to form the thyroid hormones: T4 (thyroxine) and T3
(triiodothyronine).
• Thyroglobulin Storage: The iodinated tyrosine residues remain bound to
thyroglobulin, which is stored in the colloid until needed by the body.
• Release of Hormones: When the body signals the need for thyroid hormones,
thyroglobulin is reabsorbed into the follicular cells, and enzymes break it down to
release T3 and T4 into the bloodstream.
• Deiodination: T4, the more abundant form, is converted into the more active T3
in peripheral tissues through the process of deiodination, facilitated by the enzyme
deiodinase.
• Hormone Secretion Regulation: The production and release of thyroid
hormones are regulated by the hypothalamus and pituitary gland. TSH stimulates
the thyroid to release hormones.
• Iodine Deficiency and Hormone Synthesis: A lack of iodine in the diet can
impair the thyroid’s ability to produce T3 and T4, leading to hypothyroidism and
goiter.
• Thyroid Peroxidase Role: Thyroid peroxidase is key in catalyzing the iodination
of tyrosine residues, a crucial step in the biosynthesis of thyroid hormones.
• Feedback Mechanism: High levels of T3 and T4 in the blood provide negative
feedback to the hypothalamus and pituitary, reducing TSH secretion.
• Importance of Tyrosine: Tyrosine, an amino acid, is essential for thyroid
hormone synthesis. It is part of the thyroglobulin protein and is iodinated to form
T3 and T4.
• Thyroid Hormone Storage: The thyroid gland stores sufficient quantities of T3
and T4 in thyroglobulin form to meet the body’s needs for several days.
• Thyroid Enzyme Deficiencies: Deficiencies in enzymes such as thyroid
peroxidase can lead to impaired thyroid hormone synthesis, resulting in thyroid
dysfunction.
• Regulation of Iodine Utilization: The thyroid efficiently regulates iodine uptake
to ensure sufficient hormone production, adjusting its activity according to dietary
iodine availability.
4. Control of Secretion of Thyroid Hormones

• Hypothalamus-Pituitary-Thyroid Axis: The secretion of thyroid hormones (T3

and T4) is primarily regulated by the hypothalamus and the pituitary gland
through a feedback loop. The hypothalamus releases thyrotropin-releasing
hormone (TRH), which stimulates the pituitary to release thyroid-stimulating
hormone (TSH).
• Role of TSH: TSH binds to the TSH receptors on the thyroid follicular cells,
stimulating the release of thyroid hormones. TSH is the key regulator of thyroid
hormone synthesis and secretion.
• Negative Feedback Mechanism: High levels of T3 and T4 in the blood inhibit
the secretion of TRH from the hypothalamus and TSH from the pituitary gland,
thereby reducing further hormone production.
• Environmental Factors: Factors like temperature and stress can influence the
hypothalamus and pituitary, altering the secretion of TRH and TSH.
• Iodine and Hormone Secretion: Adequate iodine is essential for the production
of thyroid hormones. Iodine deficiency leads to increased TSH secretion,
attempting to stimulate the thyroid to produce more hormones, which can lead to
goiter formation.
• Pregnancy and Hormonal Changes: During pregnancy, hCG (human chorionic
gonadotropin) can mimic TSH, leading to slightly increased thyroid hormone
production, which is normal for most pregnancies.
• Thyroid Hormone Secretion Patterns: Secretion of thyroid hormones is
typically diurnal, with higher secretion in the early morning and lower levels at
night.
• Regulation by Cortisol: Cortisol, a stress hormone, can affect thyroid function
by influencing the conversion of T4 to T3 in peripheral tissues, especially during
periods of stress.
• TRH Secretion: TRH is released from the hypothalamus in response to low
thyroid hormone levels, signaling the pituitary to release more TSH.
• TRH and TSH Secretion Disorders: In disorders such as hypothyroidism, TRH
and TSH secretion can be abnormally high due to insufficient thyroid hormone
levels.
• Cold Exposure: Cold temperatures stimulate TRH release, which increases TSH
and subsequently increases thyroid hormone production to maintain body
temperature.
• Thyroid Hormone Resistance: In rare cases, tissues may become resistant to
thyroid hormones, requiring higher levels of TSH to maintain normal thyroid
hormone levels.
• Autoimmune Diseases: In autoimmune thyroid disorders like Graves' disease,
antibodies mimic TSH and stimulate excessive thyroid hormone production,
disrupting the normal regulatory mechanisms.
• Genetic Factors: Genetic mutations affecting the TRH, TSH, or thyroid hormone
receptors can lead to abnormal thyroid hormone production and regulation.
5. Transport of Thyroid Hormones

• Binding to Plasma Proteins: The majority of thyroid hormones (T3 and T4) are
bound to plasma proteins such as thyroxine-binding globulin (TBG), transthyretin
(TTR), and albumin, which prevent them from being quickly metabolized or
excreted.
• Thyroxine-Binding Globulin (TBG): TBG is the main protein responsible for
binding T4 and, to a lesser extent, T3 in the bloodstream. About 70-80% of T4 in
circulation is bound to TBG.
• Free Hormones: A small proportion of thyroid hormones in the bloodstream is
unbound, known as free T3 and free T4. These free hormones are biologically
active and can enter cells to regulate metabolism.
• Role of Transthyretin (TTR): Transthyretin (previously called prealbumin) also
binds thyroid hormones in the blood, contributing to their transport and storage in
tissues.
• Albumin’s Role: Albumin, a common plasma protein, has a lesser affinity for
thyroid hormones but still helps in their transport through the bloodstream.
• Cellular Uptake: The free fraction of thyroid hormones enters target cells
through specific transporters on the cell membrane, such as the monocarboxylate
transporter (MCT8).
• Conversion of T4 to T3: Once inside the target cells, T4 is converted into the
more active form, T3, through the action of deiodinase enzymes.
• T3 and T4 Receptors: Once inside the cell, thyroid hormones bind to thyroid
hormone receptors in the nucleus, regulating gene expression and influencing
various metabolic processes.
• Transport to Target Tissues: Thyroid hormones circulate in the bloodstream and
are transported to tissues such as the heart, liver, muscles, and brain, where they
exert their effects on metabolism.
• Iodine Transport: Iodine is transported from the blood to the thyroid gland,
where it is used to produce thyroid hormones. Inadequate iodine leads to reduced
hormone production.
• Transport and Pregnancy: During pregnancy, thyroid hormone transport is
affected by changes in plasma proteins, which can lead to fluctuations in thyroid
hormone levels and adjustments in the fetal thyroid gland.
• Changes in Binding Proteins: Factors like pregnancy, estrogen therapy, and liver
disease can alter the levels of binding proteins, affecting the total thyroid hormone
levels in the blood.
• Thyroid Hormone Transport Disorders: In some conditions, such as familial
dysalbuminemic hyperthyroxinemia, defects in thyroid hormone-binding proteins
can lead to abnormal thyroid function and hormone levels.
• Tissue Specificity: Different tissues in the body may have varying levels of
thyroid hormone receptors and transporters, influencing how responsive they are
to thyroid hormones.
• Plasma Half-life: The plasma half-life of T4 is longer than that of T3 due to its
higher binding affinity to proteins, meaning T4 remains in circulation longer.
6. Denaturation of Thyroid Hormones

• Protein Denaturation: Thyroid hormones, like all proteins, are subject to

denaturation under certain environmental conditions such as high temperatures or
extreme pH levels.
• Effect of Heat on Thyroid Hormones: Elevated temperatures can cause the
breakdown of the tertiary structure of thyroid hormones, rendering them inactive
and unable to bind to their receptors.
• Impact of pH on Structure: Alterations in pH, such as in acidic environments,
can affect the stability of thyroid hormones, leading to loss of their biological
activity.
• Oxidative Stress: Exposure to oxidative stress or reactive oxygen species (ROS)
can cause structural changes to thyroid hormones, affecting their function.
• Enzymatic Denaturation: Certain enzymes in the liver and other organs can
degrade thyroid hormones by cleaving their peptide bonds, leading to reduced
hormonal activity.
• Denaturation in Diseases: In some thyroid disorders, such as thyroiditis,
inflammation can alter the molecular structure of thyroid hormones, impairing
their function.
• Thyroid Hormone Metabolism: The body’s natural metabolism, including
deiodination by enzymes such as deiodinase, plays a role in inactivating thyroid
hormones, ensuring they do not remain active for too long.
• Proteolytic Degradation: Thyroid hormones can undergo proteolytic cleavage in
various tissues, which can lead to the loss of biological activity or a shift in their
forms (e.g., T3 to T4 conversion).
• Pharmacological Effects: Some medications can lead to thyroid hormone
denaturation by altering the enzyme activity responsible for their synthesis or
degradation.
• Environmental Toxins: Exposure to certain environmental toxins, such as heavy
metals or pollutants, can cause denaturation of thyroid hormones, affecting their
function and leading to thyroid dysfunction.
• Denaturation in Pregnancy: Pregnancy hormones, such as estrogen, can
influence the stability and denaturation of thyroid hormones by altering the
concentrations of binding proteins and altering metabolic rates.

•
7. Physiological Roles of Thyroid Hormones

• Regulation of Metabolism: Thyroid hormones are key regulators of the basal

metabolic rate (BMR). They increase the rate of oxygen consumption and energy
expenditure in tissues.
• Growth and Development: In children, thyroid hormones are essential for the
development of the central nervous system, bones, and overall growth.
• Protein Synthesis: Thyroid hormones promote protein synthesis and influence
muscle growth by increasing the rate of amino acid uptake into cells.
• Cardiovascular Function: Thyroid hormones regulate heart rate and cardiac
output. They increase the contractility of the heart, affecting the cardiovascular
system’s efficiency.
• Thermoregulation: By influencing the metabolic rate, thyroid hormones help the
body maintain proper body temperature.
• Lipid Metabolism: These hormones regulate lipid metabolism by enhancing the
breakdown of fats and influencing the cholesterol levels in the blood.
• Carbohydrate Metabolism: Thyroid hormones promote glucose metabolism,
enhance insulin sensitivity, and increase the uptake of glucose into cells.
• Neurological Function: T3 and T4 are critical for normal brain development and
function, influencing cognition, mood, and behavior.
• Reproductive Health: Adequate thyroid hormone levels are important for
reproductive health, influencing menstrual cycles and fertility.
• Bone Health: Thyroid hormones play a role in bone growth and remodeling.
They promote the formation of bone cells and regulate calcium levels.
• Immune System Modulation: Thyroid hormones modulate immune responses
and may influence susceptibility to autoimmune diseases, such as Hashimoto’s
thyroiditis.
• Detoxification: Thyroid hormones also assist in the detoxification processes in
the liver by regulating enzymes that break down toxins.
• Sleep Regulation: Thyroid hormones influence sleep patterns by affecting
circadian rhythms and energy metabolism in the brain.
• Cholesterol Regulation: These hormones help regulate lipid profiles in the
bloodstream, contributing to a healthy balance of cholesterol.
• Body Weight: Thyroid hormones have a direct impact on body weight by
controlling metabolic rate and fat storage. Hypothyroidism can lead to weight
gain, while hyperthyroidism can cause weight loss.
8. Morphological Consequences of Excess Thyroid Hormones

• Goiter Formation: Excess thyroid hormones often lead to the enlargement of the
thyroid gland, known as a goiter, which occurs due to overstimulation of the
thyroid tissue by TSH or abnormal thyroid hormone levels.
• Thyroid Hyperplasia: In cases of hyperthyroidism, the thyroid gland undergoes
hyperplasia, leading to an increase in the number of thyroid follicular cells.
• Cardiac Hypertrophy: Chronic excess thyroid hormone can lead to cardiac
hypertrophy, where the heart muscles thicken as a compensatory response to the
increased metabolic demand.
• Skeletal Muscle Weakness: Hyperthyroidism can cause muscle wasting and
weakness due to increased protein catabolism, resulting in a reduction of muscle
mass.
• Weight Loss: Despite an increased appetite, individuals with excess thyroid
hormones may experience weight loss due to the elevated metabolic rate.
• Nervous System Alterations: The nervous system becomes hyper-excitable,
leading to symptoms like irritability, anxiety, tremors, and in severe cases,
psychiatric manifestations.
• Exophthalmos: In conditions like Graves' disease, excessive thyroid hormones
can lead to the bulging of the eyes, known as exophthalmos, due to inflammation
of the tissues behind the eyes.
• Skin Changes: Excess thyroid hormones can lead to thinning of the skin and
increased perspiration. The skin may also appear warm and moist.
• Bone Fragility: Chronic hyperthyroidism can lead to osteoporosis as a result of
increased bone resorption, making bones more fragile and prone to fractures.
• Hair and Nail Changes: There may be thinning or shedding of hair, as well as
brittle nails, due to the hypermetabolic state of the body.
• Gastrointestinal Motility: Hyperthyroidism can increase the motility of the
gastrointestinal tract, leading to diarrhea and frequent bowel movements.
• Menstrual Irregularities: Excessive thyroid hormones can lead to irregularities
in menstrual cycles, often resulting in lighter or shorter periods, or even
amenorrhea (absence of menstruation).
• Increased Sweating: Excessive sweating, especially during rest or minimal
exertion, is a common symptom of hyperthyroidism due to an elevated metabolic
rate.
• Respiratory Changes: Increased respiratory rate (tachypnea) may occur as the
body tries to meet its higher oxygen demands due to the hypermetabolic state.
9. Morphological Consequences of Deficiency of Thyroid
Hormones

• Goiter Formation: In hypothyroidism, a goiter can also form, typically due to

iodine deficiency, where the thyroid gland enlarges in an attempt to capture more
iodine to produce hormones.
• Myxedema: A common feature of hypothyroidism is the accumulation of
mucopolysaccharides in the skin and tissues, leading to a puffy appearance known
as myxedema.
• Cardiac Impairment: Hypothyroidism can lead to bradycardia (slow heart rate)
and decreased cardiac output, contributing to heart failure in severe cases.
• Muscle Weakness: Individuals with hypothyroidism often experience muscle
weakness and fatigue, particularly in the proximal muscles, due to decreased
protein synthesis and energy production.
• Weight Gain: One of the hallmark symptoms of hypothyroidism is weight gain,
due to a slowed metabolic rate, leading to increased fat storage.
• Nervous System Depression: The central nervous system becomes less
responsive, leading to symptoms such as lethargy, depression, poor memory, and
in extreme cases, coma (myxedema coma).
• Dry Skin and Hair: Skin becomes dry, rough, and thickened, while hair may
become brittle, coarse, and may fall out in patches.
• Cold Sensitivity: Hypothyroidism leads to increased sensitivity to cold
temperatures due to a reduced metabolic rate and heat production.
• Oedema: Fluid retention and swelling (oedema) are common, particularly in the
lower extremities, as the body struggles to regulate fluid balance.
• Slow Reflexes: Reflexes, particularly deep tendon reflexes, are often delayed or
sluggish in individuals with hypothyroidism.
• Constipation: Due to decreased gastrointestinal motility, constipation is common
in hypothyroid individuals.
• Menstrual Changes: Hypothyroidism can lead to heavy menstrual periods
(menorrhagia) or prolonged periods, and in severe cases, amenorrhea.
• Anemia: Hypothyroidism can contribute to anemia, particularly due to reduced
erythropoiesis (red blood cell production) in the bone marrow.
• Lipid Profile Abnormalities: Deficiency in thyroid hormones can lead to an
elevated cholesterol level, increasing the risk of atherosclerosis and
cardiovascular diseases.
• Impaired Thermogenesis: The body becomes less efficient at generating heat,
which can lead to cold intolerance and difficulty maintaining normal body
temperature.
10. Chemical Consequences of Excess Thyroid Hormones

• Increased Catabolism: Excess thyroid hormones accelerate the catabolism of

proteins, fats, and carbohydrates, leading to increased energy expenditure.
• Hyperglycemia: Due to enhanced gluconeogenesis and glycogenolysis in the
liver, excess thyroid hormones can lead to elevated blood sugar levels
(hyperglycemia).
• Hyperlipidemia: Although thyroid hormones generally regulate lipid
metabolism, excess levels can lead to elevated cholesterol and triglyceride levels,
contributing to cardiovascular risk.
• Elevated Blood Pressure: The increased metabolic rate and cardiac output lead
to a rise in systolic blood pressure, often resulting in hypertension.
• Increased Oxygen Demand: As the metabolic rate increases, there is a higher
demand for oxygen in the body, potentially leading to respiratory issues and
increased heart rate.
• Increased Thermogenesis: Excess thyroid hormones can cause excessive heat
production, leading to hyperthermia and excessive sweating.
• Protein Breakdown: Elevated thyroid hormones increase the breakdown of
proteins in muscle tissues, which can lead to muscle wasting and weakness.
• Electrolyte Imbalance: The increased metabolic rate can lead to electrolyte
imbalances, such as reduced potassium levels (hypokalemia) and sodium
retention.
• Hypercalcemia: High levels of thyroid hormones can increase the release of
calcium from bones, leading to elevated calcium levels in the bloodstream.
• Thyroid Storm: In extreme cases of hyperthyroidism, a condition known as
thyroid storm can occur, marked by severe metabolic derangements including
fever, tachycardia, and organ failure.
• Altered Liver Function: Excess thyroid hormones can affect liver function by
increasing liver enzyme activity and influencing lipid metabolism, potentially
leading to liver damage.
• Increased Adrenal Activity: Elevated thyroid hormone levels can increase
adrenal gland activity, resulting in elevated cortisol levels, which in turn affect
stress responses and immune function.
• Increased Oxygen Consumption: The body’s tissues consume more oxygen,
which can lead to an imbalance in oxygen supply and demand, causing fatigue
and increased respiratory effort.
• Bone Resorption: Excess thyroid hormones stimulate osteoclast activity, leading
to increased bone resorption and reduced bone density, increasing the risk of
fractures.
 References

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Clinical Text (9th ed.). Lippincott Williams & Wilkins.
o This textbook provides comprehensive details on the anatomy, function,
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Harper's Illustrated Biochemistry (28th ed.). McGraw-Hill.
o A detailed reference on biochemical processes, including the biosynthesis
and function of thyroid hormones.
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o Discusses the morphological changes and clinical manifestations of
hyperthyroidism, including Graves' disease.
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(7th ed.). Elsevier.
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o Provides a detailed explanation of biochemical pathways, including the
biosynthesis and regulation of thyroid hormones.
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o A comprehensive resource from the American Thyroid Association on
various thyroid disorders, diagnostic approaches, and therapeutic
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Deiodination, and Degradation. In Endocrinology (6th ed.), Elsevier.
o Detailed coverage of thyroid hormone actions, their transport, and
chemical processes in the body.
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o A valuable resource for understanding thyroid hormone dysfunction,
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deficiency.
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