Hyperthyroidism

Hyperthyroidism

Endocrine Block

Endocrine Block

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

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)