Hyperthyroidism

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Hyperthyroidism

Endocrine System

Endocrine System

Pituitary gland histology
Thyroid and parathyroid gland histology
Pancreas histology
Adrenal gland histology
Synthesis of adrenocortical hormones
Adrenocorticotropic hormone
Growth hormone and somatostatin
Hunger and satiety
Antidiuretic hormone
Thyroid hormones
Insulin
Insulins
Glucagon
Somatostatin
Cortisol
Testosterone
Estrogen and progesterone
Oxytocin and prolactin
Parathyroid hormone
Calcitonin
Vitamin D
Phosphate, calcium and magnesium homeostasis
Congenital adrenal hyperplasia
Adrenal insufficiency: Pathology review
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Cushing syndrome and Cushing disease: Pathology review
Cushing syndrome
Conn syndrome
Pheochromocytoma
Adrenal masses: Pathology review
Adrenal masses and tumors: Clinical
Adrenal cortical carcinoma
Thyroglossal duct cyst
Hyperthyroidism
Hyperthyroidism: Pathology review
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Euthyroid sick syndrome
Hypothyroidism
Hypothyroidism: Pathology review
Hashimoto thyroiditis
Hypothyroidism and thyroiditis: Clinical
Subacute granulomatous thyroiditis
Riedel thyroiditis
Thyroid storm
Thyroid nodules and thyroid cancer: Pathology review
Thyroid cancer
Thyroid nodules and thyroid cancer: Clinical
Parathyroid disorders and calcium imbalance: Pathology review
Parathyroid conditions and calcium imbalance: Clinical
Hyperparathyroidism
Hypoparathyroidism
Hypercalcemia
Hypocalcemia
Diabetes mellitus
Diabetes mellitus: Pathology review
Diabetes mellitus: Clinical
Diabetic nephropathy
Diabetic retinopathy
Pancreatic neuroendocrine neoplasms
Gigantism
Acromegaly
Hyperprolactinemia
Diabetes insipidus and SIADH: Pathology review
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Pituitary adenoma
Hypopituitarism: Pathology review
Hypopituitarism
Hyperpituitarism
Pituitary tumors: Pathology review
Pituitary apoplexy
Sheehan syndrome
Prolactinoma
Hypoprolactinemia
Constitutional growth delay
Puberty and Tanner staging
Precocious puberty
Delayed puberty
Kallmann syndrome
Disorders of sex chromosomes: Pathology review
5-alpha-reductase deficiency
Menstrual cycle
Polycystic ovary syndrome
Premature ovarian failure
Menopause
Androgen insensitivity syndrome
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia: Pathology review
Multiple endocrine neoplasia
Carcinoid syndrome
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Hyperthyroidism medications
Hypothyroidism medications
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Mineralocorticoids and mineralocorticoid antagonists
Adrenal hormone synthesis inhibitors

Transcript

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In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so hyperthyroidism refers to a condition where there’s excess thyroid hormones.

The condition is also called thyrotoxicosis, and is generally due to overproduction from the thyroid gland.

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells.

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.

Once inside the cell T­4 is mostly converted into T3, where it can exert its effect. T3 speeds up the cell’s basal metabolic rate.

So as an example, the cell might produce more proteins and burn up more energy in the form of sugars and fats.

It’s as if the cells are in a bit of frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.

Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition or when you’re trying to stay warm during a snowstorm!

Now, hyperthyroidism can happen a few different ways - all of them result in too much thyroid hormone and a hypermetabolic state, where cellular reactions are happening faster than normal.

The most common primary cause is Graves disease, an autoimmune disorder where B cells produce antibodies against several thyroid proteins.

These autoantibodies include thyroid-stimulating immunoglobulins, which bind to the TSH receptor on follicular cells and imitate TSH.

This results in growth of the thyroid gland and stimulates the follicular cells to produce excess thyroid hormone.

Another primary cause is toxic nodular goiter, where one or more follicules start generating lots of thyroid hormone - in some cases it’s because of a mutated TSH receptor that inappropriately keeps these follicular cells active.

A different cause is a hyperfunctioning thyroid adenoma, where the follicular cells start growing uncontrollably forming a benign tumor and making excess thyroid hormones.

Also, anytime the thyroid gets inflamed or damaged, there can be a large release of pre-formed thyroid hormones.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Harrison's Endocrinology, 4E" McGraw-Hill Education / Medical (2016)
  6. "Hyperthyroidism" The Lancet (2016)
  7. "Hypothyroidism and hyperthyroidism" Acta Bio Medica Atenei Parmensis (2019)